Autocrine Communication: Mode of communication wherein a bound hormone affects the function of the cell type that produced the hormone.Communication: The exchange or transmission of ideas, attitudes, or beliefs between individuals or groups.Cell Communication: Any of several ways in which living cells of an organism communicate with one another, whether by direct contact between cells or by means of chemical signals carried by neurotransmitter substances, hormones, and cyclic AMP.Animal Communication: Communication between animals involving the giving off by one individual of some chemical or physical signal, that, on being received by another, influences its behavior.Communication Disorders: Disorders of verbal and nonverbal communication caused by receptive or expressive LANGUAGE DISORDERS, cognitive dysfunction (e.g., MENTAL RETARDATION), psychiatric conditions, and HEARING DISORDERS.Health Communication: The transfer of information from experts in the medical and public health fields to patients and the public. The study and use of communication strategies to inform and influence individual and community decisions that enhance health.Communication Aids for Disabled: Equipment that provides mentally or physically disabled persons with a means of communication. The aids include display boards, typewriters, cathode ray tubes, computers, and speech synthesizers. The output of such aids includes written words, artificial speech, language signs, Morse code, and pictures.Nonverbal Communication: Transmission of emotions, ideas, and attitudes between individuals in ways other than the spoken language.Paracrine Communication: Cellular signaling in which a factor secreted by a cell affects other cells in the local environment. This term is often used to denote the action of INTERCELLULAR SIGNALING PEPTIDES AND PROTEINS on surrounding cells.Communication Barriers: Those factors, such as language or sociocultural relationships, which interfere in the meaningful interpretation and transmission of ideas between individuals or groups.Physician-Patient Relations: The interactions between physician and patient.Computer Communication Networks: A system containing any combination of computers, computer terminals, printers, audio or visual display devices, or telephones interconnected by telecommunications equipment or cables: used to transmit or receive information. (Random House Unabridged Dictionary, 2d ed)Connexin 43: A 43-kDa peptide which is a member of the connexin family of gap junction proteins. Connexin 43 is a product of a gene in the alpha class of connexin genes (the alpha-1 gene). It was first isolated from mammalian heart, but is widespread in the body including the brain.Radiology Information Systems: Information systems, usually computer-assisted, designed to store, manipulate, and retrieve information for planning, organizing, directing, and controlling administrative activities associated with the provision and utilization of radiology services and facilities.Receptors, Autocrine Motility Factor: Cell surface receptors for AUTOCRINE MOTILITY FACTOR, which is the secreted form of GLUCOSE-6-PHOSPHATE ISOMERASE. The receptor has an unusual composition in that it shares some structural similarities with G-PROTEIN-COUPLED RECEPTORS and functions as an ubiquitin protein ligase when internalized.Signal Transduction: The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.Hospital Communication Systems: The transmission of messages to staff and patients within a hospital.Interdisciplinary Communication: Communication, in the sense of cross-fertilization of ideas, involving two or more academic disciplines (such as the disciplines that comprise the cross-disciplinary field of bioethics, including the health and biological sciences, the humanities, and the social sciences and law). Also includes problems in communication stemming from differences in patterns of language usage in different academic or medical disciplines.Cell Division: The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.Cells, Cultured: Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.RNA, Messenger: RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.Communication Methods, Total: Utilization of all available receptive and expressive modes for the purpose of achieving communication with the hearing impaired, such as gestures, postures, facial expression, types of voice, formal speech and non-speech systems, and simultaneous communication.Connexins: A group of homologous proteins which form the intermembrane channels of GAP JUNCTIONS. The connexins are the products of an identified gene family which has both highly conserved and highly divergent regions. The variety contributes to the wide range of functional properties of gap junctions.Professional-Patient Relations: Interactions between health personnel and patients.Communications Media: The means of interchanging or transmitting and receiving information. Historically the media were written: books, journals, newspapers, and other publications; in the modern age the media include, in addition, radio, television, computers, and information networks.Glucose-6-Phosphate Isomerase: An aldose-ketose isomerase that catalyzes the reversible interconversion of glucose 6-phosphate and fructose 6-phosphate. In prokaryotic and eukaryotic organisms it plays an essential role in glycolytic and gluconeogenic pathways. In mammalian systems the enzyme is found in the cytoplasm and as a secreted protein. This secreted form of glucose-6-phosphate isomerase has been referred to as autocrine motility factor or neuroleukin, and acts as a cytokine which binds to the AUTOCRINE MOTILITY FACTOR RECEPTOR. Deficiency of the enzyme in humans is an autosomal recessive trait, which results in CONGENITAL NONSPHEROCYTIC HEMOLYTIC ANEMIA.Tumor Cells, Cultured: Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.Transforming Growth Factor alpha: An EPIDERMAL GROWTH FACTOR related protein that is found in a variety of tissues including EPITHELIUM, and maternal DECIDUA. It is synthesized as a transmembrane protein which can be cleaved to release a soluble active form which binds to the EGF RECEPTOR.Professional-Family Relations: The interactions between the professional person and the family.Growth Substances: Signal molecules that are involved in the control of cell growth and differentiation.Electronic Mail: Messages between computer users via COMPUTER COMMUNICATION NETWORKS. This feature duplicates most of the features of paper mail, such as forwarding, multiple copies, and attachments of images and other file types, but with a speed advantage. The term also refers to an individual message sent in this way.Interprofessional Relations: The reciprocal interaction of two or more professional individuals.Persuasive Communication: A mode of communication concerned with inducing or urging the adoption of certain beliefs, theories, or lines of action by others.Patient Satisfaction: The degree to which the individual regards the health care service or product or the manner in which it is delivered by the provider as useful, effective, or beneficial.Tape Recording: Recording of information on magnetic or punched paper tape.Vocalization, Animal: Sounds used in animal communication.Culture Media, Conditioned: Culture media containing biologically active components obtained from previously cultured cells or tissues that have released into the media substances affecting certain cell functions (e.g., growth, lysis).Nurse-Patient Relations: Interaction between the patient and nurse.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Attitude of Health Personnel: Attitudes of personnel toward their patients, other professionals, toward the medical care system, etc.Internet: A loose confederation of computer communication networks around the world. The networks that make up the Internet are connected through several backbone networks. The Internet grew out of the US Government ARPAnet project and was designed to facilitate information exchange.Telecommunications: Transmission of information over distances via electronic means.Transforming Growth Factor beta: A factor synthesized in a wide variety of tissues. It acts synergistically with TGF-alpha in inducing phenotypic transformation and can also act as a negative autocrine growth factor. TGF-beta has a potential role in embryonal development, cellular differentiation, hormone secretion, and immune function. TGF-beta is found mostly as homodimer forms of separate gene products TGF-beta1, TGF-beta2 or TGF-beta3. Heterodimers composed of TGF-beta1 and 2 (TGF-beta1.2) or of TGF-beta2 and 3 (TGF-beta2.3) have been isolated. The TGF-beta proteins are synthesized as precursor proteins.Patient Simulation: The use of persons coached to feign symptoms or conditions of real diseases in a life-like manner in order to teach or evaluate medical personnel.Role Playing: The adopting or performing the role of another significant individual in order to gain insight into the behavior of that person.Reverse Transcriptase Polymerase Chain Reaction: A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.Teleradiology: The electronic transmission of radiological images from one location to another for the purposes of interpretation and/or consultation. Users in different locations may simultaneously view images with greater access to secondary consultations and improved continuing education. (From American College of Radiology, ACR Standard for Teleradiology, 1994, p3)Questionnaires: Predetermined sets of questions used to collect data - clinical data, social status, occupational group, etc. The term is often applied to a self-completed survey instrument.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Models, Biological: Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.Gene Expression: The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.

Coexpression of transcripts encoding EPHB receptor protein tyrosine kinases and their ephrin-B ligands in human small cell lung carcinoma. (1/1262)

The EPH family is the largest subfamily of receptor protein tyrosine kinases, consisting of the EPHA and EPHB subgroups. Ephrin-B1, ephrin-B2, and ephrin-B3 are ligands of the EPHB subgroup and are encoded by the EFNB1, EFNB2, and EFNB3 genes, respectively. We have shown previously that EPHB2 transcripts are expressed in six small cell lung carcinoma (SCLC) cell lines. In this study, we examined the expression of EPHB1, EPHB2, EPHB3, EPHB4, and EPHB6 in 4 SCLC tumor specimens and 14 cell lines including 3 cell lines derived from these tumor specimens. To investigate whether potential autocrine loops of EPHB receptors and ephrin-B ligands exist in SCLC, the expression of EFNB1, EFNB2, and EFNB3 was also examined. Our data show that transcripts encoding multiple members of the EPHB subgroup and the ephrin-B subgroup are coexpressed in SCLC cell lines and tumors. These results suggest that the EPHB subgroup receptor kinases may modulate the biological behavior of SCLC through autocrine and/or juxtacrine activation by ephrin-B ligands that are expressed in the same or neighboring cells.  (+info)

Maturation, activation, and protection of dendritic cells induced by double-stranded RNA. (2/1262)

The initiation of an immune response is critically dependent on the activation of dendritic cells (DCs). This process is triggered by surface receptors specific for inflammatory cytokines or for conserved patterns characteristic of infectious agents. Here we show that human DCs are activated by influenza virus infection and by double-stranded (ds)RNA. This activation results not only in increased antigen presentation and T cell stimulatory capacity, but also in resistance to the cytopathic effect of the virus, mediated by the production of type I interferon, and upregulation of MxA. Because dsRNA stimulates both maturation and resistance, DCs can serve as altruistic antigen-presenting cells capable of sustaining viral antigen production while acquiring the capacity to trigger naive T cells and drive polarized T helper cell type 1 responses.  (+info)

Regulation of gelatinase B production in corneal cells is independent of autocrine IL-1alpha. (3/1262)

PURPOSE: The matrix metalloproteinase gelatinase B is synthesized by cells at the leading edge of the corneal epithelium migrating to heal a wound. Recent data from the authors' laboratory suggest that excessive synthesis contributes to repair defects. The goal of the study reported here was to investigate mechanisms controlling gelatinase B production by corneal epithelial cells. METHODS: Freshly isolated cultures of corneal epithelial cells and early passage stromal fibroblasts from rabbit were used for these studies. RESULTS: In a previous study, it was found that the cytokine interleukin (IL)-1alpha is released into the culture medium of corneal epithelial cells more efficiently when they are plated at low density with limited cell-cell contact than when plated at high density. In this study, we show that production of gelatinase B by these cells is similarly affected by cell plating density. However, it is further demonstrated that these two events are not dependent on one another but occur in parallel: IL-1alpha does not regulate gelatinase B production (synthesis), nor was there evidence that any other secreted autocrine cytokine acts as mediator. Instead, our data suggest that gelatinase B production is downregulated directly by high cell density and indicate a connection to the level of protein kinase C activity. Nevertheless, the anticancer agent suramin, which blocks collagenase synthesis by interfering with autocrine cytokine-receptor interactions, still inhibits synthesis of gelatinase B. CONCLUSIONS: Unlike collagenase synthesis by corneal stromal fibroblasts, production (synthesis) of gelatinase B does not appear to be controlled by secreted autocrine cytokines but can still be inhibited by suramin. Suramin may make an effective therapeutic agent for controlling pathologic overproduction of gelatinase B in corneal ulcers.  (+info)

Pituitary adenylate cyclase-activating polypeptide, interleukin-6 and glucocorticoids regulate the release of vascular endothelial growth factor in pituitary folliculostellate cells. (4/1262)

There is increasing evidence that hormones play an important role in the control of endothelial cell function and growth by regulating the production of vascular endothelial growth factor (VEGF). VEGF regulates vascular permeability and represents the most powerful growth factor for endothelial cells. In the normal anterior pituitary, VEGF has been detected only in folliculostellate (FS) cells. In the present study, the regulation of the release of VEGF from FS-like mouse TtT/GF cells, and from FS cells of rat pituitary monolayer cell cultures was investigated using a specific VEGF ELISA. Basal release of VEGF was demonstrated in cultures of both TtT/GF cells and rat pituitary cells. Interestingly, the VEGF secretion was stimulated by both forms of pituitary adenylate cyclase-activating polypeptide (PACAP-38 and PACAP-27), indicating that this hypothalamic peptide regulates endothelial cell function and growth within the pituitary. VEGF secretion was also stimulated by interleukin-6 (IL-6) whereas basal, IL-6- and PACAP-stimulated secretion was inhibited by the synthetic glucocorticoid dexamethasone. The inhibitory action of dexamethasone was reversed by the glucocorticoid receptor antagonist RU486, suggesting that in FS cells functional glucocorticoid receptors mediate the inhibitory action of glucocorticoids on the VEGF secretion. The endocrine and auto-/paracrine control of VEGF production in pituitary FS cells by PACAP, IL-6 and glucocorticoids may play an important role both in angiogenesis and vascular permeability regulation within the pituitary under physiological and pathophysiological conditions.  (+info)

Role of autocrine stimulation on the effects of cyclic AMP on protein and lipid phosphorylation in collagen-activated and thrombin-activated platelets. (5/1262)

We compared several responses in thrombin-stimulated and collagen (type I)-stimulated platelets with and without forskolin and inhibitors of autocrine stimulation (IAS: an ADP-removing system of creatine phosphate/creatine phosphokinase, Arg-Gly-Asp-Ser peptide to prevent fibrinogen/fibronectin binding to GPIIb/IIIa, SQ 29.548 as a thromboxane A2 receptor antagonist, cyproheptadine as a serotonin receptor antagonist, BN 52021 as a platelet-activating factor receptor antagonist). The pattern of tyrosine-phosphorylated proteins, the phosphorylation of lipids in the polyphosphoinositide cycle and phosphorylation of pleckstrin (P47) were studied as markers for signal-transducing responses, exposure of CD62 (P-selectin) and CD63 (Glycoprotein 53), as well as secretion of ADP + ATP and beta-N-acetyl-glycosaminidase were studied as final activation responses. Clear differences between thrombin-stimulated and collagen-stimulated platelets were observed. First, practically all protein-tyrosine phosphorylation induced by thrombin was inhibited by IAS, while a partial inhibition was observed for collagen; the phosphorylation due to collagen alone was apparently stimulated by elevation of cAMP. Secondly, the other responses to thrombin were inhibited by increased levels of cAMP, independent of autocrine stimulation. In contrast, only the autocrine part of the collagen-induced responses was inhibited by elevation of cAMP. Thus, the inhibition by elevated cAMP seen in collagen-stimulated platelets seems to be due to removal of the G-protein-mediated activation from secreted autocrine stimulators either by IAS or forskolin. The remaining activity is a pure collagen effect which is not affected by elevated levels of cAMP.  (+info)

Differential inhibition of collagenase and interleukin-1alpha gene expression in cultured corneal fibroblasts by TGF-beta, dexamethasone, and retinoic acid. (6/1262)

PURPOSE: Expression of the genes for collagenase and interleukin-1alpha (IL-1alpha) are induced as stromal cells become activated to the repair fibroblast phenotype after injury to the cornea. This investigation examines the mechanisms whereby expression of these genes is inhibited by transforming growth factor-beta (TGF-beta), dexamethasone (DEX), or retinoic acid (RET A). METHODS: A model of freshly isolated cultures of corneal stromal cells and early passage cultures of corneal fibroblasts was used in these studies. This model reproduces the events of stromal cell activation in the corneal wound. RESULTS: In early passage cultures of corneal fibroblasts, expression of collagenase is under obligatory control by autocrine IL-1alpha. IL-1alpha controls its own expression through an autocrine feedback loop that is dependent on transcription factor NF-kappaB. TGF-beta, DEX, and RET A were each effective inhibitors of collagenase gene expression in these cells. Furthermore, these agents have the capacity to inhibit expression of IL-1alpha and this was correlated with their ability to affect DNA-binding activity of NF-kappaB. However, TGF-beta, DEX, and RET A were also effective inhibitors of the low level of collagenase expressed by freshly isolated corneal stromal cells that cannot express IL-1alpha. CONCLUSIONS: In cells with an active IL-1alpha autocrine loop there are at least two distinct signaling pathways by which collagenase gene expression can be modulated. The results of this study demonstrate that TGF-beta, DEX, and RET A differentially inhibit collagenase and IL-1alpha gene expression. This information will be useful in the design of therapeutic modalities for fibrotic disease in the cornea and other parts of the eye.  (+info)

The role of macrophage cell death in tuberculosis. (7/1262)

Studies of host responses to infection have traditionally focused on the direct antimicrobial activity of effector molecules (antibodies, complement, defensins, reactive oxygen and nitrogen intermediates) and immunocytes (macrophages, lymphocytes, and neutrophils among others). The discovery of the systems for programmed cell death of eukaryotic cells has revealed a unique role for this process in the complex interplay between microorganisms and their cellular targets or responding immunocytes. In particular, cells of the monocyte/macrophage lineage have been demonstrated to undergo apoptosis following intracellular infection with certain pathogens that are otherwise capable of surviving within the hostile environment of the phagosome or which can escape the phagosome. Mycobacterium tuberculosis is a prototypical 'intracellular parasite' of macrophages, and the direct induction of macrophage apoptosis by this organism has recently been reported from several laboratories. This paper reviews the current understanding of the mechanism and regulation of macrophage apoptosis in response to M. tuberculosis and examines the role this process plays in protective immunity and microbial virulence.  (+info)

Ligation of Fc gamma RII (CD32) pivotally regulates survival of human eosinophils. (8/1262)

The low-affinity IgG Fc receptor, FcgammaRII (CD32), mediates various effector functions of lymphoid and myeloid cells and is the major IgG Fc receptor expressed by human eosinophils. We investigated whether FcgammaRII regulates both cell survival and death of human eosinophils. When cultured in vitro without growth factors, most eosinophils undergo apoptosis within 96 h. Ligation of FcgammaRII by anti-CD32 mAb in solution inhibited eosinophil apoptosis and prolonged survival in the absence of growth factors. Cross-linking of human IgG bound to FcgammaRII by anti-human IgG Ab or of unoccupied FcgammaRII by aggregated human IgG also prolonged eosinophil survival. The enhanced survival with anti-CD32 mAb was inhibited by anti-granulocyte-macrophage-CSF (GM-CSF) mAb, suggesting that autocrine production of GM-CSF by eosinophils mediated survival. In fact, mRNA for GM-CSF was detected in eosinophils cultured with anti-CD32 mAb. In contrast to mAb or ligands in solution, anti-CD32 mAb or human IgG, when immobilized onto tissue culture plates, facilitated eosinophil cell death even in the presence of IL-5. Cell death induced by these immobilized ligands was accompanied by DNA fragmentation and was inhibited when eosinophil beta2 integrin was blocked by anti-CD18 mAb, suggesting that beta2 integrins play a key role in initiating eosinophil apoptosis. Thus, FcgammaRII may pivotally regulate both survival and death of eosinophils, depending on the manner of receptor ligation and beta2 integrin involvement. Moreover, the FcgammaRII could provide a novel mechanism to control the number of eosinophils at inflammation sites in human diseases.  (+info)

Journal of Immunology Research is a peer-reviewed, Open Access journal that provides a platform for scientists and clinicians working in different areas of immunology and therapy. The journal publishes research articles, review articles, as well as clinical studies related to classical immunology, molecular immunology, clinical immunology, cancer immunology, transplantation immunology, immune pathology, immunodeficiency, autoimmune diseases, immune disorders, and immunotherapy.
Sulf-2 knockdown effect on autocrine Wnt signaling (a) H292, Calu6, and P-ST cells were transfected with TOP/FOP flash reporter system, then cultured in presenc
Insulin-like growth factors (IGFs) play an important role in the pathogenesis of several neoplasias and the IGF-binding proteins (IGFBPs) may have a role as autocrine/paracrine factors in regulating the local actions of the IGFs. In the present study we investigated IGF-I, IGF-II, IGFBP-1, IGFBP-2, and IGFBP-3 production in cultured media from three human lung cancer cell lines (Calu-3, Calu-6, A549) and in human neoplastic and normal lung tissue samples obtained at surgery from 8 patients. Calu-6 cells secreted much more IGF-II than Calu-3 and A549 (190, 25, and 5 ng/107 cells respectively) and much less IGF-I (0.7, 13, and 5 ng/107 cells). Conversely, IGFBP-1 and IGFBP-3 were most abundant in media conditioned by CALU-3 (13 and 120 ng/107 cells respectively) and least abundant in CALU-6 (,1 ng/107 cells). Molar ratio between IGF-I+IGF-II and IGFBP-1+IGFBP-3 was much higher in Calu-6 which is also the most actively replicating cell line. Regarding IGFBP-2 we found a higher concentration in ...
Spontaneous interleukin-6 (IL-6) production has been observed in various tumors and implicated in the pathogenesis, progression and drug resistance in cancer. However, the regulation of IL-6 autocrine production in cancer cells is not fully understood. IL-6 is auto-regulated in many types of cell. Two of the three major downstream pathways of IL-6, MEK/extracellular signal-related kinase (Erk) pathway and phosphatidylinositol 3-kinase (PI3-K)/Akt pathway, have been shown to regulate IL-6 expression through the activation of AP-1 and NF-κB. However, it is not clear what the role of Janus kinase (Jak) 2/signal transducer and activator of transcription (Stat) 3 pathway. This study was designed to determine the role of Jak2/Stat3 pathway in the regulation of IL-6 autocrine production in cancer cells. Inhibitors of Jak2/Stat3, MEK/Erk and PI3-K/Akt pathways down-regulated IL-6 secretion in the lung adenocarcinoma PC14PE6/AS2 (AS2) cells, which spontaneously secreted IL-6 and possessed constitutively
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Here, we demonstrated that depolarization of DMH neurons triggers the somatodendritic release of CCK, which acts as an autocrine signal to enhance NMDAR function and liberate NO. Subsequent retrograde NO signaling stimulates the release of GABA from presynaptic terminals in the DMH. These observations provide two critical pieces of information: first, they provide, to the best of our knowledge, the first report of somatodendritic release of the neuropeptide CCK in the brain. Second, they describe a novel form of synaptic regulation in which postsynaptic depolarization enhances synaptic inhibition. The latter observation is particularly intriguing because it provides an example of a feedback system in which a neuron quenches its own excitability by increasing the release of GABA from its afferents. This stands in contrast to the widespread inhibition of neurotransmitter release reported in multiple brain regions following postsynaptic depolarization and the subsequent liberation of eCBs (Wilson ...
Research: hormone/paracrine/autocrine regulation of the renal microcirculation, calcium signaling in vascular smooth muscle cells, pathophysiology of hypertension ...
Under serum-free conditions, malignant RMS cells maintain proliferation through autocrine mechanisms (21 , 57 , 59) and exhibit a relatively low level of spontaneous apoptosis, similar to that observed when cells are cultured under serum-containing conditions. These malignant cells differ, therefore, from several nonmalignant cell types, which undergo apoptosis under conditions of serum withdrawal. We showed previously that rapamycin potently induces growth arrest in Rh1 and Rh30 RMS cells under these conditions of culture. However, in the presence of serum, Rh1 cells were highly resistant to growth inhibition by rapamycin. Consequently, it was of interest to determine which components in serum protected these cells. We found that, under serum-free conditions of growth, IGF-I completely substituted for serum in causing rapamycin resistance in Rh1 cells. Exogenous IGF-I abrogated growth arrest in Rh1 cells, whereas Rh30 cells remained arrested even in the presence of IGF-I. Rescue was not due to ...
A model of autocrine signaling in cultures of suspended cells was developed on the basis of the effective medium approximation. The fraction of autocrine ligands, the mean and distribution of distances traveled by paracrine ligands before binding, as well as the mean and distribution of the ligand lifetime were derived. Interferon signaling by dendritic immune cells were considered as an illustration ...
Activation via the CD3 and CD16 pathway mediates interleukin-2-dependent autocrine proliferation of granular lymphocytes in patients with granular lymphocyte proliferative disorders. is an eagle-i resource of type Journal article at Oregon Health & Science University.
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
A large number of cells in the airways, such as eosinophils, mast cells, lymphocytes, neutrophils and ASM cells, contribute to the pathogenesis of inflammatory airway diseases. Here we specifically discuss potential anti-inflammatory interventions that target ASM-driven inflammation.. As mentioned earlier, ASM cells are potential targets for glucocorticosteroid therapy. Other workers and ourselves have recently demonstrated that the expression and secretion of pro-inflammatory cytokines and chemokines by ASM cells in vitro can be inhibited by glucocorticosteroid treatment [11,12,17,25,26,32,36,40]. COX-2 induction and the resulting production of arachidonic acid metabo-lites could similarly be inhibited by treatment with dexa-methasone [13,51]. Suppression of the COX-2 pathway, on the contrary, may result in deleterious consequences considering the bronchoprotective properties of PGE2 in asthmatic airways.. Mechanistically, it has been proposed that glucocorticoid receptors interact with ...
In this study, we showed that exogenously supplied VEGF and TGF-β rapidly increased Cx43 expression in cultured neonatal rat ventricular myocytes in a manner similar to the effects induced by brief intervals of linear pulsatile stretch. We also showed that specific antibodies against either VEGF or TGF-β blocked stretch-induced upregulation of Cx43 expression. Stretch-conditioned medium contained increased levels of VEGF and was able to stimulate Cx43 expression in cells not subjected to stretch. Anti-VEGF antibody blocked the effects of exogenous TGF-β on Cx43 expression but anti-TGF-β antibody did not block the VEGF effect. Thus, we confirmed original observations by Seko et al3 that pulsatile stretch stimulates secretion of VEGF, mediated at least in part by TGF-β, and we now provide evidence that directly implicates these pathways in stretch-mediated upregulation of Cx43.. It is likely that pulsatile stretch causes secretion of multiple mediators from cardiac myocytes and nonmyocytic ...
My research program focuses on the regulation of cholangiocyte proliferation/damage during cholangiopathies. My studies have demonstrated the key role of a number of factors such as vascular and nerve factors, melatonin, secretin, biogenic amines and sex hormones (expressed and secreted by cholangiocytes) in the regulation of biliary growth/damage by autocrine/paracrine mechanisms. Proliferating cholangiocytes display a neuroendocrine phenotype and secrete and respond to a number of hormones, neuropeptides and neurotransmitters in autocrine and paracrine signaling mechanisms. My research interests also include determining the interactions that occur between cholangiocytes and other cell types (such as hepatocytes, hepatic stellate cells, and vascular endothelial cells) in the biliary microenvironment during both cholestasis and cholangiocarcinogenesis. My program evaluates the various signaling mechanisms regulating the balance between biliary growth/damage. I have expertise in the areas of ...
Chronic inflammation and allergy involve the activation of tissue-resident cells and, later on, the invasion of effector cells. We have previously shown that the loss of phosphoinositide 3-kinase (PI3K) γ impairs chemokine-dependent migration of neutrophils and macrophages both in vitro and in vivo. On the other hand, PI3Kγ is not required either during phagocytic processes or in the activation of bactericidal activities like granule secretion and particle-mediated respiratory burst in neutrophils. Tissue mast cells are key regulators in allergy and inflammation and release histamine upon clustering of their IgE receptors. We have demonstrated that murine mast cell responses are exacerbated in vitro and in vivo by autocrine signals, and require functional PI3Kγ. Adenosine, acting through the A3 adenosine receptor, as well as other agonists of Gαi-coupled receptors, transiently increased PtdIns(3,4,5)P3 exclusively via PI3Kγ. PI3Kγ-derived PtdIns(3,4,5)P3 was instrumental for initiation of ...
Amphiregulin (AR) is a newly discovered glycosylated, 84-amino acid residue polypeptide growth regulator which has sequence homology to the EGF family of proteins. To obtain immunological reagents to study the biological role of AR, two synthetic peptides containing sequences corresponding to distinct regions of AR were used to generate polyclonal antibodies in rabbits. One preparation of antipeptide antibodies directed against residues 26-44 of AR (AR-Ab2) was most effective in the detection of native AR, whereas another preparation of antibodies against residues 8-26 (AR-Ab1) was found to be most efficacious in the detection of AR in formalin-fixed and paraffin-embedded tissues. The growth of a colon carcinoma cell line, Geo, which proliferates autonomously under serum-free conditions, was stimulated by the exogenous addition of AR or EGF. Half-maximal stimulation of this growth was observed at 40 and 200 pM of EGF and AR, respectively. A mAb to the extracellular domain of the EGF receptor ...
Autocrine signaling is a form of cell signaling in which a cell secretes a hormone or chemical messenger (called the autocrine agent) that binds to autocrine receptors on that same cell, leading to changes in the cell. This can be contrasted with paracrine signaling, intracrine signaling, or classical endocrine signaling. An example of an autocrine agent is the cytokine interleukin-1 in monocytes. When interleukin-1 is produced in response to external stimuli, it can bind to cell-surface receptors on the same cell that produced it.[citation needed] Another example occurs in activated T cell lymphocytes, i.e., when a T cell is induced to mature by binding to a peptide:MHC complex on a professional antigen-presenting cell and by the B7:CD28 costimulatory signal. Upon activation, "low-affinity" IL-2 receptors are replaced by "high-affinity" IL-2 receptors consisting of α, β, and γ chains. The cell then releases IL-2, which binds to its own new IL-2 receptors, causing self-stimulation and ...
Purified anti-human/mouse IL-21 Antibody - Interleukin 21 (IL-21) is a potent immunomodulatory cytokine mainly produced by NKT and CD4+ T-cells, particularly the inflammatory Th17 subset and has pleiotropic effects on both innate and adaptive immune responses.  These actions include positive effects such as enhancing proliferation of NK cells and cytotoxic T cells, and inhibitory effects on the antigen-presenting function of dendritic cells.  It can also be proapoptotic for B cells and NK cells.  Recent studies have shown that IL-21 is also an autocrine cytokine that potently induces T(H)17 differentiation and suppresses Foxp3 expression, and serves as a target for treating inflammatory diseases..
Purified anti-human/mouse IL-21 Antibody - Interleukin 21 (IL-21) is a potent immunomodulatory cytokine mainly produced by NKT and CD4+ T-cells, particularly the inflammatory Th17 subset and has pleiotropic effects on both innate and adaptive immune responses.  These actions include positive effects such as enhancing proliferation of NK cells and cytotoxic T cells, and inhibitory effects on the antigen-presenting function of dendritic cells.  It can also be proapoptotic for B cells and NK cells.  Recent studies have shown that IL-21 is also an autocrine cytokine that potently induces T(H)17 differentiation and suppresses Foxp3 expression, and serves as a target for treating inflammatory diseases..
Takaoka et al. have presented persuasive evidence that in MEFs the IFN-γ response is substantially augmented through autocrine IFN-α/β and that cross-recruitment and phosphorylation of the IFNAR1 subunit of the IFN-α/β receptor occurs in response to IFN-γ in these cells (24). We have been unable to obtain evidence for or against recruitment or phosphorylation of IFNAR1 in response to IFN-γ in the HT1080-based human cell systems used here (H. Isharc and I. M. Kerr, unpublished data). In a potentially analogous but inverse situation, cross-phosphorylation of the IFNGR1 subunit of the IFN-γ receptor in response to activation of erythropoietin/gp130 receptor chimeras in HT1080-based cell lines is observed. Importantly, however, such receptor cross-phosphorylation plays no part in the IFN-γ-like response observed (23), a result which emphasizes that even if IFNAR1 were recruited and phosphorylated in response to IFN-γ, proof of necessity of this for the IFN-γ antiviral response would ...
Despite the considerable improvements in our knowledge of AML biology in recent years, the treatment of this disease remains a challenge for clinicians. Major efforts have been made to develop new compounds that target the preferentially activated signaling pathways implicated in AML cell proliferation and survival. The PI3K/Akt/mTOR axis represents a promising therapeutic target in several cancers, as many components of these signaling pathways are frequently deregulated in tumor cells. We recently showed that a constitutive activation of PI3K is detected in ∼50% of primary AML samples at diagnosis(8), mostly due to an autocrine stimulation of the IGF-1 receptor (9). Accordingly, either the blockade of this IGF-1 autocrine production or the specific inhibition of PI3K p110δ activity leads to a strong decrease of AML cell proliferation (4, 5, 9). The constitutive activation of the mTORC1 pathway is detectable in virtually almost all AML patient samples, which emphasized the potential of using ...
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For several years there has been considerable interest in stimulating angiogenesis by a variety of growth factors, including the family of fibroblast growth factors (FGF). FGF-5 is a protooncogene known to stimulate cell growth and proliferation in multiple cell types, including cancer.1 The cardiac myocyte can also produce different isoforms of FGFs, eg, it has been shown that the expression of basic FGF increases in hibernating myocardium,2 which was the disease state of interest in the current study published in Circulation Research.3 The most commonly cited effect of FGF-5 in the heart is to promote angiogenesis. Several studies have shown that gene transfer of FGF-5 in the heart increases vessel formation and regional blood flow.4-6 This effect is mediated by a production of FGF-5 by the cardiac myocytes, followed by its release in the extracellular space. In addition, FGF-5 can function as an autocrine/paracrine mechanism of cardiac cell growth and as a cytoprotective mechanism against ...
Lipoxygenases (EC 1.13.11.-) are a family of (non-heme), iron-containing enzymes most of which catalyze the dioxygenation of polyunsaturated fatty acids in lipids containing a cis,cis-1,4- pentadiene into cell signaling agents that serve diverse roles as autocrine signals that regulate the function of their parent cells, paracrine signals that regulate the function of nearby cells, and endocrine signals that regulate the function of distant cells. The lipoxygenases are related to each other based upon their similar genetic structure and dioxygenation activity. However, one lipoxygenase, ALOXE3, while having a lipoxygenase genetic structure, possesses relatively little dioxygenation activity; rather its primary activity appears to be as an isomerase that catalyzes the conversion of hydroperoxy unsaturated fatty acids to their 1,5-epoxide, hydroxyl derivatives. Lipoxygenases are found in eukaryotes (plants, fungi, animals, protists); while the third domain of terrestrial life, the archaea, ...
Phlogistic reactions, whether of extraocular or intraocular origin, tend to be down regulated by the avascular, and hence immune privileged, cornea. And this feature is recognised as being essential for a favourable graft prognosis. In situ, corneal tissue is protected from potential inflammatory stimulants, such as endotoxins, by the epithelial and vascular barriers; but in vitro, the situation is different. Under these conditions, contamination of culture media with endotoxins could have untoward effects; these may be manifested either directly, by overt changes in cell morphology, and/or by a more discreet influence on the tissues immunological status, the consequences of which may be realised only after transplantation, by a compromised graft performance.. In the current study, we monitored the media of organ cultured corneas for a number of cytokine mediators of the inflammatory response, both before and after spiking with endotoxin; these data were then compared with those pertaining to ...
article{99c2b32e-f9cf-4afb-8052-6d71d776ad00, abstract = {The first lineage commitment step of hematopoietic stem cells (HSC) results in separation into distinct lymphoid and myeloid differentiation pathways, reflected in the generation of common lymphoid and myeloid progenitors (CLP and CMP, respectively). In this report we present the first evidence for a nonredundant regulator of this process, in that adult mice deficient in expression of the flt3 ligand (FL) have severely (10-fold) reduced levels of the CLP, accompanied by reductions in the earliest identifiable B and T cell progenitors. In contrast, CMP and HSC are unaffected in FL-deficient mice. Noteworthy, CLP express high levels of both the flt3 receptor and ligand, indicating a potential autocrine role of FL in regulation of the earliest lymphoid commitment step from HSC.}, author = {Sitnicka Quinn, Ewa and Bryder, David and Theilgaard-Mönch, Kim and Buza-Vidas, Natalija and Adolfsson, Jörgen and Jacobsen, Sten Eirik W}, issn = ...
Our hypothesis is based on several lines of evidence. First, the effects of cAMP and DA on both 4xCRE (Figs. 3a,b, 5) and c-fos and BDNF mRNA expression (Fig. 6) are blocked by NMDAR antagonists. Second, two structurally distinct inhibitors of neuronal EAA uptake, TBOA (Fig. 7) and trans-PDC (supplemental Fig. S3, available at www.jneurosci.org as supplemental material), potentiated the stimulation of gene transcription by cAMP. Third, the aspartate+glutamate-, but not the glutamate-only-, scavenging system abolished stimulation of CREB-dependent gene transcription by forskolin (Fig. 8); the aspartate-scavenging enzyme, GOT, degrades l- but not d-aspartate demonstrating that l-aspartate is the active extracellular EAA in this signaling pathway. Finally, forskolin was found to induce release of aspartate but not glutamate (Fig. 9). Together, these results lead to the conclusion that cAMP-induced release of aspartate and the resulting activation of NR2B-containing NMDARs mediate the effects of ...
Looking for online definition of autocrine in the Medical Dictionary? autocrine explanation free. What is autocrine? Meaning of autocrine medical term. What does autocrine mean?
1. Jemal A, Bray F, Center MM, Ferlay J, Ward E, Forman D. Global cancer statistics. CA Cancer J Clin. 2011;61:69-90 2. Bosetti C, Turati F, La Vecchia C. Hepatocellular carcinoma epidemiology. Best Pract Res Clin Gastroenterol. 2014;28:753-770 3. Li S, Sun R, Chen Y, Wei H, Tian Z. TLR2 limits development of hepatocellular carcinoma by reducing IL18-mediated immunosuppression. Cancer Res. 2015;75:986-995 4. Naugler WE, Sakurai T, Kim S, Maeda S, Kim K, Elsharkawy AM, Karin M. Gender disparity in liver cancer due to sex differences in MyD88-dependent IL-6 production. Science. 2007;317:121-124 5. He G, Dhar D, Nakagawa H, Font-Burgada J, Ogata H, Jiang Y, Shalapour S, Seki E, Yost SE, Jepsen K, Frazer KA, Harismendy O, Hatziapostolou M, Iliopoulos D, Suetsugu A, Hoffman RM, Tateishi R, Koike K, Karin M. Identification of liver cancer progenitors whose malignant progression depends on autocrine IL-6 signaling. Cell. 2013;155:384-396 6. Gu FM, Li QL, Gao Q, Jiang JH, Zhu K, Huang XY, Pan JF, Yan J, ...
Nitric oxide-generating system as an autocrine mechanism in human polymorphonuclear leucocytes.: Recent data [Lopéz-Farré, Riesco, Moliz, Egido, Casado, Hernand
Programmed cell death has a vital role in embryonic development and tissue homeostasis. oxygen varieties (ROS) in tuberculosis illness. Experimental studies have also demonstrated that upregulation of RIPK3 and MLKL detected in alcoholic and drug-induced liver injury suggests that necroptosis is also involved in sterile inflammation. Application of Necrostatin (Nec)-1 or depletion of RIPK3 protects liver cells from these types of injuries [74]. Parasitic diseases like leishmaniasis and malaria generally caused hemolysis, Lenalidomide supplier anemia, and sometimes bleeding. These result due to rupturing of red blood corpuscles (RBCs) leading to release of hemoglobin (Hb) into circulation; heme is produced on oxidation of Hb leading to initiation of the Fenton reaction and culminates with generation of ROS. Heme is also responsible for direct activation of TLR4, leading to autocrine secretion of ROS and TNF, and they activate the RIPK1/3-dependent necroptosis in a synergistic manner [75]. In ...
Gonadotropin-releasing hormone (GnRH) is a decapeptide hormone secreted by GnRH neurons located in the hypothalamus. It is responsible for the onset of puberty and the regulation of hormone release from the pituitary. There is a strong evidence suggesting that these GnRH neurons are intrinsically capable of generating pulsatile and episodic neurosecretion of this hormone. However, the underlying mechanism for the GnRH-pulse generator remains obscure. The discovery of GnRH receptors allowing GnRH to exert autocrine regulation on its own release, led several experimentalist in NIH to propose in 2003 a mechanism underlying this effect. We developed in 2006 a mathematical model describing the proposed mechanism, then we extended it to explain synchrony observed in GnRH neurons by incorporating the idea of a common pool of GnRH hormone. In this talk, we shall present this model and analyze several aspects of it, especially robustness. We shall show that the coupling of a heterogeneous family of GnRH ...
2390 Janus kinase 2 (JAK2) is a cytokine receptor associated tyrosine kinase. Binding of cytokines to their specific receptors leads to their dimerization and activation of associated JAKs. Activated JAKs phosphorylate specific tyrosine residues in the cytoplasmic chains of the receptor, which now act as docking sites for SH2 containing latent transcription factors known as STATs. Once bound to the receptor, STATs are activated by JAKs through phosphorylation of their tyrosine residues. Activated STATs form stable dimers and translocate to the nucleus, where they bind specific promoter sequences of their target genes involved in cell proliferation and survival, such as Bcl-xL, Bcl-2, c-myc and cyclin D1. Tumor cell lines and samples derived from hematopoetic malignancies (leukemia, lymphoma and multiple myeloma) and solid tumors (breast, head and neck, lung, prostrate and ovarian cancers) exhibit deregulated JAK-STAT signaling, which can be attributed to autocrine cytokine production or growth ...
NovoPro offers a wide selection of tools for research on cytokines and their receptors. These include high-purity recombinant proteins, high-specific antibodies and ORF cDNA clones.. Cytokines are a large group of proteins, peptides or glycoproteins that are secreted by specific cells of immune system. Cytokines are a category of signaling molecules that mediate and regulate immunity, inflammation and hematopoiesis. Cytokines are produced throughout the body by cells of diverse embryological origin. Cytokine is a general name; other names are defined based on their presumed function, cell of secretion, or target of action. For example, cytokines made by lymphocytes can also be referred to as lymphokines, while interleukins are made by one leukocyte and act on other leukocytes. And chemokines are cytokines with chemotactic activities.. Cytokines may act on the cells that secrete them (autocrine action), on nearby cells (paracrine action), or in some instances on distant cells (endocrine ...
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VEGF-A promoted DJM-1 cell proliferation via NRP1 in an autocrine manner. (A) A western blot shows that DJM-1 cells expressed NRP1, but not NRP2. DJM-1 cells we
Comoglio, P.M., 1988: Autocrine activation of the tyrosine kinase associated with the bombesin receptor in small cell lung carcinoma
Dictyostelium cells secrete the proteins AprA and CfaD. Cells lacking either AprA or CfaD proliferate faster than wild type, while AprA or CfaD overexpressor cells proliferate slowly, indicating that AprA and CfaD are autocrine factors that repress proliferation. CfaD interacts with AprA and requires the presence of AprA to slow proliferation. To determine if CfaD is necessary for the ability of AprA to slow proliferation, whether AprA binds to cells, and if so whether the binding requires the presence of CfaD, we examined the binding and effect on proliferation of recombinant AprA. We find that the extracellular accumulation of AprA increases with cell density and reaches a concentration of 0.3 μg/ml near a stationary cell density. When added to wild-type or aprA- cells, recombinant AprA (rAprA) significantly slows proliferation at 0.1 μg/ml and higher concentrations. From 4 to 64 μg/ml, the effect of rAprA is at a plateau, slowing but not stopping proliferation. The proliferation-inhibiting
alpha(1B)-Adrenergic receptors mediate many of the actions of the natural catecholamines, adrenaline and noradrenaline. They belong to the seven transmembrane domains G protein-coupled receptor superfamily and exert their actions mainly through activation of Gq proteins and phosphoinositide turnover/calcium signaling. Many hormones and neurotransmitters are capable of inducing alpha(1B)-adrenergic receptor phosphorylation and desensitization; among them: adrenaline and noradrenaline, phorbol esters, endothelin-I, bradykinin, lysophosphatidic acid, insulin, EGF, PDGF, IGF-I, TGF-beta, and estrogens. Key protein kinases for these effects are G protein coupled receptor kinases and protein kinase C. The lipid/protein kinase, phosphoinositide-3 kinase also appears to play a key role, acting upstream of protein kinase C. In addition to the agents employed for cells stimulation, we observed that paracrine/autocrine mediators also participate; these processes include EGF transactivation and ...
As potential autocrine or paracrine factors, extracellular nucleotides are known to be important regulators of renal ion transporters by activating cell surface receptors and intracellular signaling pathways. We investigated the influence of extracellular adenine nucleotides on Na+/H+ exchanger isoform 3 (NHE3) activity in A6-NHE3 cells. This is a polarized cell line obtained by stable transfection of A6 cells with the cDNA encoding the rat isoform of NHE3, which is expressed on the apical membrane. Basolateral addition of the P2Y(1) agonist, 2-Me-SADP, induced an inhibition of NHE3 activity, which was prevented by preincubation with selective P2Y(1) antagonists, MRS 2179 (N-6-methyl-2-deoxyadenosine-3,5-bisphosphate) and MRS 2286 (2-[2-(2-chloro-6-methylamino-purin-9-yl)-ethyl]-propane- 1,3-bisoxy(diammoniumphosphate)). NHE3 activity was also significantly inhibited by ATP and ATP-gamma-S but not by UTP. 2-Me-SADP induced a P2Y(1) antagonist-sensitive increase in both [Ca2+]i and cAMP ...
The RAF inhibitor vemurafenib (PLX4032) increases survival in patients with BRAF-mutant metastatic melanoma, but has limited efficacy in patients with colorectal cancers. Thyroid cancer cells are also comparatively refractory to RAF inhibitors. By contrast to melanomas, inhibition of MAPK signaling by vemurafenib is transient in thyroid and colorectal cancer cells. The rebound in ERK in thyroid cells is accompanied by increased HER3 signaling caused by induction of HER3 transcription through decreased promoter occupancy by the transcriptional repressors CtBP1 and 2, and by autocrine secretion of neuregulin-1. The HER kinase inhibitor lapatinib prevents MAPK rebound and sensitizes BRAF-mutant thyroid cancer cells to RAF or MEK inhibitors. This provides a rationale for combining ERK pathway antagonists with inhibitors of feedback-reactivated HER signaling in this disease. The determinants of primary resistance to MAPK inhibitors vary between cancer types, due to preferential upregulation of ...
Eosinophils are major effector cells in type 2 inflammatory responses and become activated in response to IL-4 and IL-33, yet the molecular mechanism remains unclear. We examined the direct effect of these cytokines on eosinophils and demonstrated that murine eosinophils respond to IL-4 and IL-33 by phosphorylation of STAT-6 and NFkB, respectively. RNA sequencing analysis of murine eosinophils indicated that IL-33 regulates 519 genes, whereas IL-4 regulates only 28 genes, including 19 IL-33-regulated genes. Interestingly, IL-33 induced eosinophil activation via two distinct mechanisms, IL-4 independent and IL-4 secretion/auto-stimulation dependent. Anti-IL-4 or anti-IL-4Ra antibody-treated eosinophils, as well as Il4- or Stat6-deficient eosinophils, had attenuated protein secretion of a subset of IL-33-induced genes, including Retnla and Ccl17. However, the induction of most IL-33-regulated transcripts (e.g. Il6 and Il13) was IL-4 independent and blocked by NFkB inhibition. Indeed, IL-33 induced the
Th17 cells are critically involved in autoimmune disease induction and severity. Recently, we showed that Th17 cells from patients with rheumatoid arthritis (RA) directly induced a proinflammatory loop upon interaction with RA synovial fibroblasts (RASF), including increased autocrine IL-17A production. To unravel the mechanism driving this IL-17A production, we obtained primary CD4+CD45RO+CCR6+ (Th17) cells and CD4+CD45RO+CCR6− (CCR6−) T cells from RA patients or healthy individuals and cocultured these with RASF. IL-1β, IL-6, IL-23p19, and cyclooxygenase (COX)-2 expression and PGE2 production in Th17-RASF cultures were higher than in CCR6− T cell-RASF cultures. Cytokine neutralization showed that IL-1β and IL-6, but not IL-23, contributed to autocrine IL-17A induction. Importantly, treatment with celecoxib, a COX-2 inhibitor, resulted in significantly lower PGE2 and IL-17A, but not IFN-γ, production. Combined celecoxib and TNF-α blockade more effectively suppressed the ...
Epithelial cells are unable to grow or survive when they lose contact with appropriate ECM proteins. However, transformation by the Ras oncoprotein bypasses the need for signals from adhesion receptors and protects them from undergoing apoptosis. Ras‐dependent survival in other systems is known to have two effectors, PI 3‐K and Raf, the latter of which functions by activating the ERK (a MAPK) pathway. To address the contribution of ERK, J. Downward (London, UK) used an inducible active form of Raf to monitor early changes in gene transcription that impart protection from detachment‐induced apoptosis. Among the genes that are strongly up‐regulated by activated Raf are the autocrine factors HB‐EGF, amphiregulin and TGFα. All of these are members of the epithelial growth factor (EGF) family, indicating that protection by Raf is dependent on the function of an autocrine loop involving transcriptional induction of cell survival EGF‐like factors. Interestingly, Raf‐dependent survival is ...
In light of the poor control of malignant mesothelioma by approved cytotoxic chemotherapeutic regimens, RTKs have been actively explored in MPM as alternative therapeutic targets (15, 19, 42, 43). Although EGFR, VEGFRs, MET, and PDGFRs have been a focus in these studies, our findings support the novel role of FGFR1 as a growth driver in a subset of MPM cell lines and suggest that FGFR-active TKIs may serve as therapeutics in this cancer. RNAi-mediated silencing of FGFR1 inhibited clonogenic growth of two FGFR1-expressing MPM cell lines, H226 and MSTO211H (Fig. 4), and the TKI, ponatinib, selectively inhibited growth of MPM cell lines expressing FGFR1 (Fig. 2). We previously demonstrated with RNAi-mediated silencing the requirement of FGF2 for H226 cell growth (35), and we validate this finding by showing sensitivity of FGFR1-dependent mesothelioma cell lines to the ligand trap, FP-1039. Combined, the data support the activity of an FGF-FGFR1 autocrine pathway in a subset of mesothelioma cell ...
Platelet-derived growth factor (PDGF), a potent mitogen for mesenchymal cells, elicits its effects by binding to cell surface tyrosine kinase receptors, denoted α- and β-receptors. This thesis describes the mechanism of interaction between stimulated PDGF receptors and various intracellular molecules.. PDGF-B is homologous to the transforming protein v-sis encoded by the simian sarcoma virus (SSV). Transformation of cells by the v-sis oncogene occurs through an autocrine mechanism, whereby the v-Sis protein produced by a cell activates the cells own PDGF receptors. We investigated the subcellular location of the autocrine signal and found that in c-Sis/B-chain transformed cells, autophosphorylated intracellular receptors initiated activation of phosphatidylinositol 3 kinase, and tyrosine phosphorylation of phospholipase C-γ (PLC-γ) and Ras GTPase-activating protein (RasGAP). These signals were, however, not sufficient for transformation of the cells.Receptor-association with Grb2 and SHP-2, ...
The present study examined the EP subtypes involved. In primary cultures of rat IMCD cells, EP4 antagonism with structurally distinct EP4 antagonists completely abolished Ang II-induced PRR expression, and EP4 agonism alone elevated the expression. In Sprague-Dawley rats, EP4 antagonism effectively suppressed the increases in renal medullary PRR expression, renal medullary and urinary renin levels, as well as blood pressure in response to Ang II infusion. Interestingly, in vitro data also suggested involvement of the EP1 but not the EP3 subtype in Ang II-induced PRR expression.. PGE2 is a major prostanoid produced in the kidney, particularly in the CD. As an autocrine/paracrine factor, PGE2exerts a diverse range of action at the site of its production, affecting renal medullary blood flow and tubular sodium and water transport, as well as cell survival.26,27 The biological action of PGE2 is mediated by 4 distinct EP4 receptors (EP1-4). We for the first time demonstrated a dominant role of the ...
Cytokines are small, secreted, glycoproteins that specifically affect the interactions and communications between cells. Cytokines are produced transiently and locally, acting in a paracrine or autocrine manner, and they are extremely potent, ligating high affinity cell surface receptors to elicit changes in gene expression and protein synthesis in the responding cell. Cytokines produced during the differentiation of T follicular helper (Tfh) cells and B cells within the germinal center (GC) niche play an important role in ensuring that the humoral immune response is robust, whilst retaining flexibility, during the generation of affinity matured antibodies. Cytokines produced by B cells, antigen presenting cells and stromal cells are important for the differentiation of Tfh cells and Tfh cell produced cytokines act both in an autocrine fashion to firm Tfh cell differentiation and in a paracrine fashion to support the differentiation of memory B cells and plasma cells. In this review, we discuss the role
The transforming growth factor α (TGFα) epidermal growth factor receptor (EGFR) autocrine pathway plays a key role in the development and progression of human epithelial cancers (1). Overexpression of TGFα and/or EGFR has been detected in the majority of human carcinomas, has been associated with resistance to cytotoxic drugs and to hormone therapy, and is generally an indicator of poor prognosis (1). For these reasons, the blockade of the EGFR-driven autocrine pathway has been proposed as a target for anticancer therapy (2). Several pharmacologic approaches have been developed for blocking EGFR. The two most successful approaches for the treatment of cancer patients have been thus far the anti-EGFR-blocking monoclonal antibodies (MAb), such as Cetuximab, and the selective EGFR small molecule tyrosine kinase inhibitors (TKI), such as Gefitinib and Erlotinib (3-5).. Tumor angiogenesis is the process leading to the formation of blood vessels within a tumor and plays a key role in cancer cell ...
IFN-γ is a well-characterized macrophage differentiation signal. Macrophages pretreated with IFN-γ achieve a higher level of activation, e.g., IFN-γ-primed macrophages become more sensitive to other stimuli, such as bacterial products and cytokines, as evidenced by the synergistic induction of many inflammatory gene products, e.g., iNOS (12)(35)(36) and IL-12 p40 (13)(37)(42)(43). In this paper, we show that activation with IFN-γ, as well as its priming effect, can be extended to Cox-2, another gene with a central role in inflammatory responses. Although IFN-γ regulation of Cox-2 has been described previously (26)(44)(45), little is known of the molecular mechanisms that underlie activation of this gene by IFN-γ. For example, in bronchial epithelial cells (44) and in normal human epidermal keratinocytes (26), Cox-2 induction is controlled through autocrine loops via the epidermal growth factor receptor and its ligands, such as TGF-α, resulting in a delayed activation. However, in ...
JAK/STAT3 is one of the major signaling pathways that is aberrantly activated in ovarian cancer and associated with tumor progression and poor prognosis in patients with ovarian cancer. In this study, we evaluated the therapeutic potential of targeting JAK/STAT3 signaling in ovarian cancer using a peritoneal dissemination mouse model. We developed this mouse model by injecting a metastatic human ovarian cancer cell line, SKOV3-M-Luc, into the peritoneal cavity of immunodeficient mice. This model displayed a phenotype similar to late-stage ovarian cancer, including extensive peritoneal metastasis and ascites production. The constitutive activation of STAT3 in human ovarian cancer cells appeared to be mediated by an autocrine cytokine loop involving the IL6 family of cytokines and JAK1 kinase. shRNA-mediated knockdown of JAK1 or STAT3 in ovarian cancer cells led to reduced tumor growth, decreased peritoneal dissemination, and diminished ascites production, suggesting a critical role of STAT3 in ...
Cytokines Cytokines are a group of regulatory proteins critically involved in many physiological processes such as immune recognition, cell differentiation and cell proliferation. They have been identified in many vertebrate species and are produced by a variety of different cell types. Cytokines are usually produced transiently and locally, acting in a paracrine or autocrine manner. They interact with high affinity cell surface receptors specific for each cytokine or cytokine group and are active at very low concentrations mostly in the picogram range.
Cytokines Cytokines are a group of regulatory proteins critically involved in many physiological processes such as immune recognition, cell differentiation and cell proliferation. They have been identified in many vertebrate species and are produced by a variety of different cell types. Cytokines are usually produced transiently and locally, acting in a paracrine or autocrine manner. They interact with high affinity cell surface receptors specific for each cytokine or cytokine group and are active at very low concentrations mostly in the picogram range.
Background. Hepatocyte growth factor (HGF) is a potent regenerative factor involved in wound healing. Previous studies have shown that mesenchymal cells produce HGF, stimulating epithelial cells in a paracrine fashion.. Objective. To examine whether autocrine HGF production by keratinocytes can occur upon skin injury.. Methods. A 31-year-old male patient sustained a burn affecting 80% of his total body surface area. Biopsies were taken from intact skin near the injured area, and skin keratinocytes were separated and cultured. Conditioned medium from keratinocytes was analyzed for HGF by ELISA, surface plasmon resonance (SPR), and dot blotting. Binding of HGF from conditioned medium to its receptor, c-Met, was compared with recombinant HGF by SPR. Finally, we examined the motogenic effect on mouse transformed skin epithelial cells (CCL-53.1) of HGF from conditioned medium.. Results. HGF was detected in the cultured keratinocyte medium. Similar to recombinant HGF, HGF from conditioned medium had a ...
Dendritic cells (DCs)3 undergo a composite program in response to microbial components, referred to as maturation. Maturing DCs up-regulate the membrane expression of molecules involved in T cell activation and costimulation, including MHC class I and class II CD40, CD80, and CD86 molecules. This process is necessary for productive activation of naive T cells, which takes place in the lymph nodes (1).. DCs committed to maturation in peripheral tissues reach the lymph nodes through afferent lymphatic vessels: they release inflammatory chemokines, which induce through an autocrine/paracrine loop the down-regulation of the CCR1 and CCR5 chemokine receptors (2). Later on, DCs up-regulate the expression of CCR7 and CXCR4, thus acquiring responsiveness to lymph node chemokines. DCs that do not express CCR7 cannot reach the lymph nodes. Conversely, DC migration abates in mice lacking lymph node chemokines or the γ-isoform of phosphoinositide-3 kinase, which is required for response to chemotactic ...
Work performed over the past 15 years has shown that the endothelium acts as a dietary salt sensor that responds to changes in salt intake. This effect is mediated through endothelial BKCa channel activity, which regulates not only the development of a signalosome complex composed of Pyk2, c-Src, and PI3K but also promotes a decrease in endothelial PTEN levels.1,3-8,21-24 PTEN is a phosphatase that counteracts the production of PIP3 by PI3K. Decreasing PTEN levels, therefore, facilitates the activity of PI3K, which regulates Akt activation through the generation of intracellular PIP3.9-12 One net effect of increased dietary salt intake is augmented endothelial production of TGF-β and potentially bioavailable NO.3 Building on these findings, the data in the present study demonstrated that (1) dietary salt induced endothelial cell production of TGF-β, which promoted an autocrine function on endothelial cells mediated through TGF-β receptor I/activin receptor-like kinase 5 and the Smad signaling ...
In America and Western Europe, prostate cancer is the second leading cause of death in men. Emerging evidence suggests that chronic inflammation is a major risk factor for the development and metastatic progression of prostate cancer. We previously reported that the chemopreventive polyphenol curcumin inhibits the expression of the proinflammatory cytokines CXCL1 and -2 leading to diminished formation of breast cancer metastases. In this study, we analyze the effects of curcumin on prostate carcinoma growth, apoptosis and metastasis. We show that curcumin inhibits translocation of NFκB to the nucleus through the inhibition of the IκB-kinase (IKKβ, leading to stabilization of the inhibitor of NFκB, IκBα, in PC-3 prostate carcinoma cells. Inhibition of NFκB activity reduces expression of CXCL1 and -2 and abolishes the autocrine/paracrine loop that links the two chemokines to NFκB. The combination of curcumin with the synthetic IKKβ inhibitor, SC-541, shows no additive or synergistic ...
Vascular endothelial growth factor (VEGF) was originally identified as an endothelial cell specific growth factor stimulating angiogenesis and vascular permeability. Some family members, VEGF C and D, are specifically involved in lymphangiogenesis. It now appears that VEGF also has autocrine functions acting as a survival factor for tumour cells protecting them from stresses such as hypoxia, chemotherapy and radiotherapy. The mechanisms of action of VEGF are still being investigated with emerging insights into overlapping pathways and cross-talk between other receptors such as the neuropilins which were not previously associated with angiogenesis. VEGF plays an important role in embryonic development and angiogenesis during wound healing and menstrual cycle in the healthy adult. VEGF is also important in a number of both malignant and non-malignant pathologies. As it plays a limited role in normal human physiology, VEGF is an attractive therapeutic target in diseases where VEGF plays a key role. It was
Cell to cell via gap junctions. Chemical messengers in ECF: neural (neurotransmitters at synapses), endocrine (hormones and growth factors), paracrine (products of cells diffuse to neighbours), Autocrine = cell secretes messenger that acts on itself. Same chemical can function in several ways. Juxtacrine = molecules attached to membrane that attaches to another cell.. ...
Not too much going on at the moment- just gearing up for Christmas. Ive done almost all the Christmas shopping, we just have to get a present for Shanes Dad, and I need help with that one! Boys are so hard to shop for! Mind you, in saying that, I think I married the easiest man to shop for ever! Because Shane has so many interests you can always think of something to get him.... he loves music and plays the bass, ukulele, piano, drums and guitar, with the bass being his first and main instrument and the rest being ones he is picking up and learning along the way. He also loves computers and design- hes constantly getting calls from somebody asking for help with their computer, and he designed our churchs website this year. He also loves gardening and is starting our veggie garden, plus he is very interested in all things Biblical. He listens to Chuck Missler and Chuck Smith an awful lot, especially when hes driving, and he loves reading biblical commentaries and historical commentaries. ...
Polycystic kidney disease is characterized by slow expansion of fluid-filled cysts derived from tubules within the kidney. Cystic expansion results in injury to surrounding parenchyma and leads to inflammation, scarring, and ultimately loss of renal function. Macrophages are a key element in this process, promoting cyst epithelial cell proliferation, cyst expansion, and disease progression. Previously, we showed that the microenvironment established by cystic epithelial cells can program macrophages, inducing M2-like macrophage polarization characterized by expression of markers that include Arg1 and Il10. Here, we functionally characterize these macrophages, demonstrating that their differentiation enhances their ability to promote cyst cell proliferation. This observation suggests a model of reciprocal, pathologic interactions between cysts and the innate immune system: cyst epithelial cells promote macrophage polarization to a phenotype that, in turn, is especially efficient in promoting ...
In the present study we examined the capacity of interleukin-1 (IL-1) α, β, interleukin-1 receptor antagonist (IL-1ra) and follicle stimulating hormone (FSH) to induce transferrin secretion by Sertoli cells under in vitro conditions. Primary Sertoli cell (SC) cultures from immature mice secreted constitutively transferrin. Stimulation of these cultures with IL-1α, IL-1β significantly increas\d their capacity to secrete transferrin. Addition of IL-1ra to unstimulated SC cultures did not affect their capacity to secrete transferrin. Stimulation of SC cultures with a combination of both IL-1α and FSH or IL-1β and FSH showed additive effect between IL-1 and FSH in their capacity to induce transferrin secretion by these cells. However, stimulation of Sertoli cells with a combination of both IL-1ra and FSH did not affect their capacity to secrete transferrin compared with FSH-stimulated cultures. Our results may suggest the involvement of testicular paracrine/autocrine factors (IL-1) and ...
Autocrine Action of Thrombospondin-2 Determines the Chondrogenic Differentiation Potential and Suppresses Hypertrophic Maturation of Human Umbilical Cord Blood-Derived Mesenchymal Stem Cells
The functional consequences of angiopoietin/Tie-2 signaling have been well established through genetic loss-of-function and gain-of-function experiments (Carmeliet, 2003; Maisonpierre et al., 1997; Suri et al., 1996; Yancopoulos et al., 2000). The phenotypes of Ang-1- and Ang-2-deficient and -overexpressing mice have led to an agonistic Ang-1/Tie-2 model and an antagonistic Ang-2/Tie-2 model (Hanahan, 1997). According to these, Ang-1 activates Tie-2 and induces subsequent signal transduction promoting endothelial-cell survival, endothelial quiescence and vessel assembly. Conversely, Ang-2 is believed to act as a non-signal-transducing Tie-2 ligand that binds to endothelial Tie-2 and thereby negatively interferes with agonistic Ang-1/Tie-2 functions. As such, it does not exert functions of its own but rather acts as a facilitator of other vascular cytokines. The net outcome of Ang-2 functions is therefore considered to be contextually determined by the presence of other cytokines. For example, ...
Endothelin is the most potent constrictor of human blood vessels known to man. In mammals, there are three structurally and pharmacologically separate ET isopeptides: ET-1, ET-2, and ET-3 (Volpe 46). Endothelin-1 is the primary isoform in the human cardiovascular system and is a 21-amino acid peptide produced chiefly by endothelial cells (Lüscher 2434). Endothelin-converting enzymes (ECE), chymases, and non-ECE metalloproteases are responsible for the synthesis of ET-1 by means of autocrine regulation (Lüscher 2434). ET-1 operates through the initiation of two G-protein coupled receptors: ETA and ETB. Located on vascular smooth muscle cells, ETA receptors regulate vasoconstriction and cell proliferation. ETB receptors, situated on endothelial cells, mediate endothelium-dependent vasodilation through the release of nitric oxide and prostacyclin (Haapaniemi 721). In addition to its cardiovascular and mitogenic effects, endothelin-1 is involved in gastrointestinal and endocrine function, ...
TY - JOUR. T1 - DLC1 negatively regulates angiogenesis in a paracrine fashion. AU - Shih, Yi Ping. AU - Liao, Yi Chun. AU - Lin, Yuan. AU - Lo, Su Hao. PY - 2010/11/1. Y1 - 2010/11/1. N2 - The Rho GTPase-activating protein DLC1 is a tumor suppressor that is often deleted in liver cancer and downregulated in other cancers. DLC1 regulates the actin cytoskeleton, cell shape, adhesion, migration, and proliferation through its Rho GTPase-activating protein activity and focal adhesion localization. In this study, we silenced DLC1 in nonmalignant prostate epithelial cells to explore its tumor suppression functions. Small hairpin RNA-mediated silencing of DLC1 was insufficient to promote more aggressive phenotypes associated with tumor cell growth. In contrast, DLC1 silencing promoted pro-angiogenic responses through vascular endothelial growth factor (VEGF) upregulation, accompanied by the accumulation of hypoxia-inducible factor 1α and its nuclear localization. Notably, modulation of VEGF expression ...
TY - JOUR. T1 - Chronic pancreatitis. T2 - a path to pancreatic cancer. AU - Pinho, Andreia V.. AU - Chantrill, Lorraine. AU - Rooman, Ilse. PY - 2014/4/10. Y1 - 2014/4/10. N2 - Chronic pancreatitis predisposes to pancreatic cancer development and both diseases share a common etiology. A central role has been proposed for the digestive enzyme-secreting acinar cell that can undergo ductal metaplasia in the inflammatory environment of pancreatitis. This metaplastic change is now a recognised precursor of pancreatic cancer. Inflammatory molecules also foster tumour growth through autocrine and paracrine effects in the epithelium and the stroma.These insights have raised new opportunities such as the manipulation of inflammation as a preventive and/or therapeutic strategy for pancreatic cancer. Finally, we address the need for an in-depth study of the pancreatic acinar cells.. AB - Chronic pancreatitis predisposes to pancreatic cancer development and both diseases share a common etiology. A central ...
Phosphoinositide 3-kinase γ (PI3Kγ) plays a major role in chronic inflammation and allergy. It is a heterodimer of a catalytic p110γ subunit and an adaptor protein, either p101 or the p101 homolog p84 (p87PIKAP). It is unclear whether both PI3Kγ complexes specifically modulate responses such as chemotaxis and degranulation. In mast cells, the p84:p110γ complex synergizes with immunoglobulin E (IgE)- and antigen-clustered FcɛRI receptor signaling and is required to achieve maximal degranulation. During this process, PI3Kγ is activated by ligands of heterotrimeric guanine nucleotide-binding protein (G protein)-coupled receptors (GPCRs), in particular adenosine receptors, through autocrine and paracrine pathways. Here, we show that p110γ needs p84 to relay signals from GPCRs to formation of phosphatidylinositol 3,4,5-trisphosphate [PtdIns(3,4,5)P3], phosphorylation of Akt, migration of cells, and synergistic adenosine-enforced degranulation. Furthermore, the absence of adaptor subunits ...
NSL3 could also have important endocrine or paracrine roles in other tissues. Although defective spermatogenesis found in INSL3 or LGR8 null mice could be the secondary effects of cryptorchidism, Leydig cell-derived INSL3 could play a paracrine role in the testis because LGR8 is also expressed in the testis. In females, INSL3 is expressed in the luteal cells of the ovary through the estrous cycle and during pregnancy [1] ...
Hmc Shantha Kumara, PhD, Hiromichi Miyagaki, MD, Xiaohong Yan, PhD, Myers A Elizabeth, MD, Sonali A C Herath, BS, Joon J Jang, MD, Linda Njoh, MS, Vesna Cekic, RN, Richard L Whelan, MD. Division of Colon and Rectal Surgery, Department of Surgery, St Luke-Roosevelt Hospital Center, Suite 7B, 425 West, 59th Street, New York, NY 10019, USA. Introduction: Minimally invasive colorectal resection (MICR) for cancer results in persistently elevated levels of plasma VEGF, Angiopoietin 2, sVCAM-1, PlGF and other proangiogenic proteins. Plasma from 2nd and 3rd week after MICR stimulates in-vitro endothelial cell (EC) migration, invasion and EC tube formation. The proangiogenic plasma after MICR may stimulate residual cancer growth after surgery. Various cancers (colon, breast, prostate, etc) and endothelial cells (EC) have been shown to express IL8 (CXCR8) and its receptors CXCR1 and CXCR2. Tumor derived IL8, in an autocrine fashion, enhances tumor cell proliferation and survival and also promotes ...
The University of Auckland Library Trefoil Factor-1 (TFF1) belongs to the family of trefoil factor peptides. Trefoil factors protect the gastrointestinal tract against mucosal injury. Trefoil peptides are upregulated and secreted in an autocrine and paracrine fashion in response to gastrointestinal injury. They facilitate cell migration and prevent anoikis. TFF1 is also expressed in various tissues and regulated by multiple cellular processes. Several studies have also demonstrated increased expression of TFF1 in a high percentage of mammary and prostate carcinoma cases. However, the functional role of autocrine TFF1 in mammary and prostate carcinoma has not been previously elucidated. Herein, I demonstrate that forced expression of TFF1 in mammary carcinoma cells resulted in increased total cell number as a consequence of increased cell proliferation and survival. Forced expression of TFF1 enhanced anchorage-independent growth and promoted scattered cell morphology with increased cell migration ...
TY - JOUR. T1 - A renal dopamine-1 receptor defect in two genetic models of hypertension. AU - Felder, R. A.. AU - Kinoshita, S.. AU - Sidhu, A.. AU - Ohbu, K.. AU - Kaskel, Frederick J.. PY - 1990. Y1 - 1990. N2 - Dopamine (DA), via DA-1 receptors, regulates Na+ transport in the kidneys. Dopamine is synthesized from L-DOPA in the proximal tubule and presumably secreted as an autocrine/paracrine substance to stimulate DA-1 receptors localized on proximal tubular cells. We have previously reported the presence of DA-1 receptors in renal cortical homogenates and on the isolated proximal tubule of the rat and rabbit, consistent with the dopamine autocrine/paracrine model. We have localized DA-1 receptors in the proximal straight tubule of the rabbit, and in the cortical collecting duct of the rabbit and rat, but not in the distal collecting tubule or the cortical thick ascending loop of Henle. The presence of functional DA-1 receptors has been substantiated by the coexistence of DA-1 ...
Versnel MA, Claesson-Welsh L, Hammacher A, Bouts MJ, van der Kwast TH, Eriksson A, Willemsen R, Weima SM, Hoogsteden HC, Hagemeijer A, et al., Human malignant mesothelioma cell lines express PDGF β-receptors whereas cultured normal mesothelial cells express predominantly PDGF α-receptors. Oncogene 1991; 6: 2005-11 ...
Takagi, Y.; Fukase, M.; Takata, S.; Yoshimi, H.; Tokunaga, O.; Fujita, T. (1990-04-30) «Autocrine effect of endothelin on DNA ... synthesis in human vascular endothelial cells» Biochemical and Biophysical Research Communications (2): 537-543 ISSN 0006-291X ...
Islets can influence each other through paracrine and autocrine communication, and beta cells are coupled electrically to six ...
Biochemical and Biophysical Research Communications. 261 (3): 756-65. doi:10.1006/bbrc.1999.1039. PMID 10441498.. ... LMW FGF2 is primarily cytoplasmic and functions in an autocrine manner, whereas HMW FGF2s are nuclear and exert activities ... Biochemical and Biophysical Research Communications. 274 (2): 337-43. doi:10.1006/bbrc.2000.3142. PMID 10913340.. ...
Paracrine signaling is a form of cell-cell communication in which a cell produces a signal to induce changes in nearby cells, ... Autocrine signaling is a form of cell signaling in which a cell secretes a hormone or chemical messenger (called the autocrine ... and that cooperation of autocrine PDGFR signaling with oncogenic was required for survival during EMT. Autocrine PDGFR ... Autocrine signaling plays critical roles in cancer activation and also in providing self-sustaining growth signals to tumors.[ ...
Gastric-brain communication is an essential part of energy homeostasis, and several communication pathways are probable, ... autocrine modulators in health and disease". Clinical and Experimental Pharmacology & Physiology. 37 (1): 125-31. doi:10.1111/j ... Biochemical and Biophysical Research Communications. 374 (1): 60-63. doi:10.1016/j.bbrc.2008.06.114. PMID 18611393.. ... Biochemical and Biophysical Research Communications. 280 (1): 132-38. doi:10.1006/bbrc.2000.4065. PMID 11162489.. ...
"Nature Communications. 1 (7): 100. Bibcode:2010NatCo...1E.100W. doi:10.1038/ncomms1093. PMC 3186516. PMID 20981028.. ...
This can result from changes in presynaptic calcium as well as feedback onto presynaptic receptors, i.e. a form of autocrine ... mapping to the transmitter-based characterization of the neuronal networks leading to two modes of brain communication: wiring ...
Biochemical and Biophysical Research Communications. 233 (3): 592-600. doi:10.1006/bbrc.1997.6509. PMID 9168896.. ...
2002). "General Principles of Cell Communication". In NCBI bookshelf. Molecular biology of the cell (4th ed.). New York: ... Other types of cell signaling include paracrine signalling and autocrine signalling. Contents. ... cell communication.[2] Cells use mainly the receptor integrin to interact with ECM proteins. This signaling can influence the ...
The autocrine or paracrine secretion of IL-2 can bind to that same Th cell or neighboring Th's via the IL-2R thus driving ... B cell maturation and function by engaging CD40 on the B cell surface and therefore facilitating cell-cell communication.[3] A ... which acts upon itself in an autocrine fashion. Activated T cells also produce the alpha sub-unit of the IL-2 receptor (CD25 or ...
The SCN coordinates daily timekeeping in the body and VIP plays a key role in communication between individual brain cells ... Conconi MT, Spinazzi R, Nussdorfer GG (2006). "Endogenous ligands of PACAP/VIP receptors in the autocrine-paracrine regulation ...
"A BDNF autocrine loop in adult sensory neurons prevents cell death". Nature. 374 (6521): 450-53. Bibcode:1995Natur.374..450A. ... and cognitive stimulation all translates into more neuronal activity and synaptic communication, which can produce structural ...
... and can also function as an autocrine signal. Depending on cell type, it can drive adaptive/developmental changes requiring ... "Nature Communications. 6 (8046): 8046. doi:10.1038/ncomms9046. PMC 4569695. PMID 26345128.. ...
PTHrP acts as an endocrine, autocrine, paracrine, and intracrine hormone. It regulates endochondral bone development by ... Biochemical and Biophysical Research Communications. 282 (2): 629-34. doi:10.1006/bbrc.2001.4607. PMID 11401507.. ...
This definition holds for most "classical" hormones, but there are also paracrine mechanisms (chemical communication between ... cells within a tissue or organ), autocrine signals (a chemical that acts on the same cell), and intracrine signals (a chemical ...
Biochemical and Biophysical Research Communications. 179 (1): 190-6. doi:10.1016/0006-291X(91)91353-E. PMID 1883350.. ... Biochemical and Biophysical Research Communications. 154 (2): 765-72. doi:10.1016/0006-291X(88)90206-9. PMID 3261170.. ...
It is maintained as a stem cell layer through an autocrine signal, TGF-a, and through paracrine signal FGF7 aka keratinocyte ... chemical communication, even anti-bacterial/viral properties for protection against pathogens.[15] ...
GABA is synthesized by neurons and acts both as an autocrine (acting on the same cell) and paracrine (acting on nearby cells) ... Nature Communications. 6: 7750. Bibcode:2015NatCo...6E7750K. doi:10.1038/ncomms8750. PMID 26177896. Valeeva G, Tressard T, ...
Inhibition of cytokine receptor synthesis and blockade of the autocrine and paracrine actions of cytokines and PGE2 were also ... Biochemical and Biophysical Research Communications. 261 (1): 214-217. doi:10.1006/bbrc.1999.1010. PMID 10405348. Cheng, Z. N ...
These attributes make nitric oxide ideal for a transient paracrine (between adjacent cells) and autocrine (within a single cell ... Biochemical and Biophysical Research Communications. 157 (1): 87-94. doi:10.1016/S0006-291X(88)80015-9. PMID 3196352. Wallace ...
As such, succinate links TCA cycle dysfunction or metabolic changes to cell-cell communication and to oxidative stress-related ... Autocrine succinate signaling promotes retinal neovascularization, triggering the activation of angiogenic factors such as ... Cell Communication and Signaling. 14: 3. doi:10.1186/s12964-016-0126-1. PMC 4709936 . PMID 26759054. Bardella, Chiara; Pollard ...
... autocrine communication MeSH G04.335.122.155 --- bystander effect MeSH G04.335.122.300 --- embryonic induction MeSH G04.335. ... 122.600 --- paracrine communication MeSH G04.335.122.850 --- signal transduction MeSH G04.335.122.850.580 --- ...
... and acts as an autocrine factor to induce apoptosis in endothelial cells. This cytokine is also found to inhibit endothelial ... Biochemical and Biophysical Research Communications. 364 (1): 1-6. doi:10.1016/j.bbrc.2007.09.097. PMID 17935696. ...
Biochemical and Biophysical Research Communications. 420 (2): 428-33. doi:10.1016/j.bbrc.2012.03.012. PMID 22426480. Yang P, ... metabolites made and released by nearby cells to act as paracrine signals for coordinating responses between cells or autocrine ... Biochemical and Biophysical Research Communications. 274 (2): 377-82. doi:10.1006/bbrc.2000.3152. PMID 10913346. Nilsson NE, ... Biochemical and Biophysical Research Communications. 274 (2): 383-8. doi:10.1006/bbrc.2000.3153. PMID 10913347. Yokomizo T, ...
Nature Communications. 5. doi:10.1038/ncomms4338. PMC 3966078 . PMID 24569435. Najm, F. J.; Lager, A. M.; Zaremba, A.; Wyatt, K ... "Autocrine signaling based selection of combinatorial antibodies that transdifferentiate human stem cells". PNAS. 110: 8099-8104 ... Nature Communications. 4: 2307. doi:10.1038/ncomms3307. PMID 23942048. Tamer M. A. Mohamed, Nicole R. Stone, Emily C. Berry, et ... Nature Communications. 7: 10080. doi:10.1038/ncomms10080. PMC 4729817 . PMID 26733021. Akinci, E; Banga, A; Tungatt, K; et al ...
In multicellular organisms, signal transduction pathways have evolved to regulate cell communication in a wide variety of ways ... First messengers are the signaling molecules (hormones, neurotransmitters, and paracrine/autocrine agents) that reach the cell ... while the terms autocrine and paracrine began to be used. Sutherland was awarded the 1971 Nobel Prize in Physiology or Medicine ... Biochemical and Biophysical Research Communications. 319 (1): 1-11. doi:10.1016/j.bbrc.2004.04.150. PMID 15158434. Wolanin PM, ...
There is massive communication between the blastocyst and the endometrium at this stage. The blastocyst signals to the ... It secretes several autocrine factors, targeting itself and stimulating it to further invade the endometrium. Furthermore, ... This communication is conveyed by receptor-ligand-interactions, both integrin-matrix and proteoglycan ones. Another ligand- ... Human chorionic gonadotropin is an autocrine growth factor for the blastocyst. Insulin-like growth factor 2, on the other hand ...
C. Interleukin 1 is an autocrine secreted by helper T cells. D. Both interleukin 2 is an autocrine secreted by cytotoxic T ... Business Communication Building Critical Skills 6th Canadian Edition By Braun Locker -Test Bank ... D. Both interleukin 2 is an autocrine secreted by helper T cells and interleukin 1 is a cytokine are true. E. All of the ... A. Interleukin 2 is an autocrine secreted by cytotoxic T cells. B. Interleukin 1 is a paracrine secreted by macrophages and B ...
VEGFR2 autocrine feed-forward loop triggers angiogenesis in lung cancer Oncogenic BRAF regulates oxidative metabolism via PGC1α ... a novel biomarker for early diagnosis Communication through resonance in spiking neuronal networks Bleb-driven chemotaxis of ... opening a new channel of communication between cells and machines Prostaglandin e2 increases hematopoietic stem cell survival ... and heterosynaptic plasticity Autocrine BDNF TrkB signalling within a single dendritic spine Mycoplasma pneumoniaetriggering ...
Intervention: Improving Communication В· Encourage choice of and attendance at communication habilitation program to sanction ... and the mutual intracellular signalling is activated in both cell populations highlighting autocrine and paracrine actions of ... Communication and Lingua franca Expansion The property of language allows the preschool child to put forth thoughts and ... Unencumbered, unestablished, reputable communication and discussion are fundamental to commend a trim, efficient relationship. ...
Unraveling the chemokine-driven communication pathways in this complex process could possibly lead to new therapeutic ... Chemokines, a family of chemoattractive proteins, have been suggested to be key players in cell-to-cell communication and ... Endothelial cells differentially express functional CXC-chemokine receptor-4 (CXCR-4/fusin) under the control of autocrine ... Chemokines, a family of chemoattractive proteins, have been suggested to be key players in cell-to-cell communication and ...
Autocrine Communication / drug effects * Autocrine Communication / physiology* * Biological Factors / metabolism* * Biological ... Inhibitory Autocrine Factors Produced by the Mesenchyme-Derived Hair Follicle Dermal Papilla May Be a Key to Male Pattern ...
Ehrlich tumor cells stimulate T-cell production of interferon-gamma and are resistant to autocrine nitric oxide ... in the UK counties of Shropshire and Staffordshire overwhelmingly sought doctors with good personal qualities and communication ...
Furthermore, we showed that GM-CSF was a driver for VEGF release by CEC in autocrine and/or paracrine manners through the ... Communication and information sharing at VA facilities during the 2009 novel H1N1 influenza pandemic. ... and how communication differs by age. Activation of group I metabotropic glutamate receptors depresses recurrent inhibition of ...
This has led to evaluation of paracrine and autocrine actions of prolactin at these tissues and a possible role in development ... BRIEF COMMUNICATIONS. Panhypopituitarism with empty sella a sequel of pituitary hyperplasia due to chronic primary ...
M. Tokunou, T. Niki, K. Eguchi et al., "c-MET expression in myofibroblasts: role in autocrine activation and prognostic ... Biochemical and Biophysical Research Communications, vol. 377, pp. 114-119, 2008. View at: Publisher Site , Google Scholar*Q. ... Biochemical and Biophysical Research Communications, vol. 280, pp. 788-797, 2001. View at: Publisher Site , Google Scholar*A. ...
Smad7 inhibits autocrine expression of TGF-β2 in intestinal epithelial cells in baboon necrotizing enterocolitis. Namachivayam ... Nature communications. 10, 1, 3494.. Research output: Contribution to journal › Article ...
Communication of this knowledge to the relatives and the professional caregivers allows an adequate adaptation of the human and ... of tumour cell lines derived from BKV/tat-transgenic mice by modulating the production of both uPA and PAI-1 via autocrine and ...
17beta-estradiol antagonizes cardiomyocyte hypertrophy by autocrine/paracrine stimulation of a guanylyl cyclase A receptor- ...
Autocrine Communication* / drug effects * Autocrine Communication* / genetics * Cell Line, Tumor * Cell Proliferation / drug ... Autocrine Activation of the MET Receptor Tyrosine Kinase in Acute Myeloid Leukemia Nat Med. 2012 Jul;18(7):1118-22. doi: ... Our results show a widespread dependence of AML cells on autocrine activation of MET, as well as the key role of compensatory ... We found HGF expression leading to autocrine activation of its receptor tyrosine kinase, MET, in nearly half of the AML cell ...
Pregnant women have high serum concentrations of sex steroid hormones, which are major regulators of paracrine and autocrine ...
This definition holds for most "classical" hormones, but there are also paracrine mechanisms (chemical communication between ... cells within a tissue or organ), autocrine signals (a chemical that acts on the same cell), and intracrine signals (a chemical ...
Thus either autocrine or paracrine mechanisms may become active. Figure B-3 summarizes a model of the possible mechanism. At ... Biochemical and Biophysical Research Communications 260:522-526.. Loo, D.T., M.C. Althoen, and C.W. Cotman 1995 Differentiation ... Biochemical and Biophysical Research Communications 186:944-950.. Benzi, G., and A. Moretti 1995 Are reactive oxygen species ...
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Notes over cell communication in chapter 9 of the text book, covering internal receptors, cell-surface receptors, autocrine ... Notes over cell communication in chapter 9 of the text book, covering internal receptors, cell-surface receptors, autocrine ... Notes over cell communication in chapter 9 of the text book, covering internal receptors, cell-surface receptors, autocrine ... Over Metabolism, Cellular Respiration, Photosynthesis, and Cell Communication. Specific details about Calvin cycle, citric acid ...
Such communication can be accomplished in two ways. Cells may physically touch each other, relaying information via specific ... Critical autocrine growth factor for T cells; increases killing of tumors by NK cells (creating LAK cells). ... Cytokines may exert their varied effects in an autocrine (acting on the cell from which they were secreted), paracrine (acting ...
Communications from God were related to current events rather than to the prediction of future events. As a result, the number ... Their role as autocrine or paracrine growth factors and their effects on surrounding nonneoplastic stroma may suggest a means ...
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Autocrine inhibition of cell motility can drive epithelial branching morphogenesis in absence of growth. Elisabeth G. Rens, ... MET Receptor Tyrosine Kinase Regulates Vagal Laryngeal Motor Neuron Development and Lifespan Ultrasonic Vocal Communication. ...
STAT3-RANTES autocrine signaling is essential for tamoxifen resistance in human breast cancer cells. Mol Cancer Res. 2013;11:31 ... the EGFR/ERK signaling pathway and upregulation of β1-integrin expression which is responsible for the enhanced communications ... have tested the hypothesis that tamoxifen resistance results from genetic alterations and autocrine or paracrine mechanisms in ...
"These journals provide researchers with a platform for rapid, open access scientific communication. The articles are of high ... NOX4 mediates hypoxia-induced proliferation of human pulmonary artery smooth muscle cells: the role of autocrine production of ... interesting possibilities to disseminate openly and freely new knowledge and even to facilitate interpersonal communication ...
taxonomy, constitute the basis for applications and scientific communication: reliable identification and correct naming of ... induction of tumor stromal cells to produce paracrine growth factors or could involve cancer cell autonomous autocrine and/or ...
  • UCSF studies show that autocrine feedback loop among STAT3, EGFR and NF-KB mediates primary resistance and suggest combinatorial therapy to treat EGFR-amplified glioblastomas. (cancer.gov)
  • This is a heteroregulatory phenomenon that could allow for intercompartmental communication, providing a tighter linkage of different cellular populations. (glowm.com)
  • Upon malignant transformation in different cancer types, the dysregulation of these connexin and pannexin channels and their effect in cellular communication, can either enhance or suppress tumorigenesis and metastasis. (biomedcentral.com)
  • G. M. Hu , C. Y. Lee , Y.-Y. Chen , N. N. Pang and W. J. Tzeng , Mathematical model of heterogeneous cancer growth with an autocrine signalling pathway, Cell Prolif , 45 (2012), 445-455. (aimsciences.org)
  • Tat affects the fibrinolytic activity of tumour cell lines derived from BKV/tat-transgenic mice by modulating the production of both uPA and PAI-1 via autocrine and paracrine mechanisms of action. (faintpower.tk)