Vascular Endothelial Growth Factor C
Vascular Endothelial Growth Factor Receptor-3
Vascular Endothelial Growth Factor A
Endothelial Growth Factors
Vascular Endothelial Growth Factor D
Vascular Endothelial Growth Factors
Lymphatic Metastasis
Vascular Endothelial Growth Factor Receptor-2
Receptors, Vascular Endothelial Growth Factor
Lymphokines
Vascular Endothelial Growth Factor Receptor-1
Neovascularization, Pathologic
Neovascularization, Physiologic
Receptors, Growth Factor
Angiogenesis Inhibitors
Immunohistochemistry
Vascular Endothelial Growth Factor B
Receptor Protein-Tyrosine Kinases
Fibroblast Growth Factor 2
Endothelium, Vascular
Endothelial Cells
RNA, Messenger
Cells, Cultured
Hypoxia-Inducible Factor 1, alpha Subunit
Replication Protein C
Neuropilin-1
Intercellular Signaling Peptides and Proteins
Angiogenesis Inducing Agents
Signal Transduction
Angiopoietin-1
Epidermal Growth Factor
Mice, Nude
Angiopoietin-2
Rosacea
Erythema
Facial Dermatoses
Telangiectasis
Drug Eruptions
VEGFR-3 and its ligand VEGF-C are associated with angiogenesis in breast cancer. (1/512)
Recently, monoclonal antibodies against the human vascular endothelial growth factor receptor VEGFR-3 were shown to provide a specific antigenic marker for lymphatic endothelium in various normal tissues. In this study we have investigated the expression of VEGFR-3 and its ligand VEGF-C in normal breast tissue and in breast tumors by immunohistochemistry. VEGFR-3 was weakly expressed in capillaries of normal breast tissue and in fibroadenomas. In intraductal breast carcinomas, VEGFR-3 was prominent in the "necklace" vessels adjacent to the basal lamina of the tumor-filled ducts. VEGF receptor 1 and 2 as well as blood vessel endothelial and basal lamina markers were colocalized with VEGFR-3 in many of these vessels. Antibodies against smooth muscle alpha-actin gave a weak staining of the necklace vessels, suggesting that they were incompletely covered by pericytes/smooth muscle cells. A highly elevated number of VEGFR-3 positive vessels was found in invasive breast cancer in comparison with histologically normal breast tissue (P < 0.0001, the Mann-Whitney test). VEGF-C was located in the cytoplasm of intraductal and invasive cancer cells. The results demonstrate that the expression of VEGFR-3 becomes up-regulated in the endothelium of angiogenic blood vessels in breast cancer. The results also suggest that VEGF-C secreted by the intraductal carcinoma cells acts predominantly as an angiogenic growth factor for blood vessels, although this paracrine signaling network between the cancer cells and the endothelium may also be involved in modifying the permeabilities of both blood and lymphatic vessels and metastasis formation. (+info)Vascular endothelial growth factor-C expression in human prostatic carcinoma and its relationship to lymph node metastasis. (2/512)
Lymph node dissemination is a major prognostic factor in human cancer. However, the molecular mechanisms underlying lymph node metastasis are poorly understood. Recently, vascular endothelial growth factor-C (VEGF-C) was identified as a ligand for VEGF receptor-3 (VEGFR-3/Flt-4) and the expression of VEGFR-3 was found to be highly restricted to the lymphatic endothelial cells. In this report, we investigated the expression of VEGF-C and VEGFR-3 in human prostatic carcinoma tissue by using in situ hybridization and immunohistochemical staining respectively. Expression of VEGF-C mRNA in prostatic carcinoma was significantly higher in lymph node-positive group than in lymph node-negative group. In addition, the number of VEGFR-3-positive vessels was increased in stroma surrounding VEGF-C-positive prostatic carcinoma cells. These results suggest that the expression of VEGF-C in prostatic carcinoma cells is implicated in the lymph node metastasis. (+info)Role of vascular endothelial growth factor C expression in the development of lymph node metastasis in gastric cancer. (3/512)
Neogenesis of lymphatic vessel and lymphatic invasion is frequently found in the stroma of cancers, but the mechanisms of this phenomenon remain unclear. Vascular endothelial growth factor C (VEGF-C) is known to be the only growth factor for the lymphatic vascular system, and its receptor has been identified as Flt4. To clarify the mechanism of lymphatic invasion in cancer, we studied the expression of VEGF-C and flt4 genes in gastric cancer tissues. VEGF-C mRNA was mainly expressed in primary tumors (15 of 32; 47%), but the frequency of VEGF-C mRNA expression was low in normal mucosa (4 of 32; 13%). In primary tumors, there was a significant relationship between VEGF-C and flt4 mRNA expression. In contrast, Flt4 was mainly expressed on the lymphatic endothelial cells but not in cancer cells. A strong correlation was found between VEGF-C expression and lymph node status, lymphatic invasion, venous invasion, and tumor infiltrating patterns. Cancer cells in the lymphatic vessels frequently showed intracytoplasmic VEGF-C immunoreactivity. Furthermore, there was a close correlation between VEGF-C tissue status and the grade of lymph node metastasis. Patients with high expression of VEGF-C protein had a significantly poorer prognosis than did those in low VEGF-C expression group. By the Cox regression model, depth of wall invasion, lymph node metastasis, and VEGF-C tissue status emerged as independent prognostic parameters, and the VEGF-C tissue status was ranked third as an independent risk factor for death. These results strongly suggest that cancer cells producing VEGF-C may induce the proliferation and dilation of lymphatic vessels, resulting in the development of invasion of cancer cells into the lymphatic vessel and lymph node metastasis. (+info)Vascular endothelial growth factor-C stimulates the migration and proliferation of Kaposi's sarcoma cells. (4/512)
Recent evidence suggesting vascular endothelial growth factor-C (VEGF-C), which is a regulator of lymphatic and vascular endothelial development, raised the question whether this molecule could be involved in Kaposi's sarcoma (KS), a strongly angiogenic and inflammatory tumor often associated with infection by human immunodeficiency virus-1. This disease is characterized by the presence of a core constituted of three main populations of "spindle" cells, having the features of lymphatic/vascular endothelial cells, macrophagic/dendritic cells, and of a mixed macrophage-endothelial phenotype. In this study we evaluated the biological response of KS cells to VEGF-C, using an immortal cell line derived from a KS lesion (KS IMM), which retains most features of the parental tumor and can induce KS-like sarcomas when injected subcutaneously in nude mice. We show that VEGFR-3, the specific receptor for VEGF-C, is expressed by KS IMM cells grown in vitro and in vivo. In vitro, VEGF-C induces the tyrosine phosphorylation of VEGFR-2, a receptor also for VEGF-A, as well as that of VEGFR-3. The activation of these two receptors in KS IMM cells is followed by a dose-responsive mitogenic and motogenic response. The stimulation of KS IMM cells with a mutant VEGF-C unable to bind and activate VEFGR-2 resulted in no proliferative response and in a weak motogenic stimulation, suggesting that VEGFR-2 is essential in transducing a proliferative signal and cooperates with VEGFR-3 in inducing cell migration. Our data add new insights on the pathogenesis of KS, suggesting that the involvement of endothelial growth factors may not only determine KS-associated angiogenesis, but also play a critical role in controlling KS cell growth and/or migration and invasion. (+info)Vascular endothelial growth factor (VEGF) and VEGF-C show overlapping binding sites in embryonic endothelia and distinct sites in differentiated adult endothelia. (5/512)
Vascular endothelial growth factor (VEGF) is a key modulator of angiogenesis during development and in adult tissues, whereas the related VEGF-C has been shown to induce both lymphangiogenesis and angiogenesis. To better understand the specific functions of these growth factors, we have here analyzed their binding to sections of mouse embryonic and adult tissues and compared the distribution of the bound growth factors with the expression patterns of the 3 known members of the VEGF receptor family as well as with neuropilin-1, a coreceptor for VEGF(165). Partially overlapping patterns of VEGF and VEGF-C binding were obtained in embryonic tissues, consistent with the expression of all known VEGF receptors by vascular endothelial cells. However, the most striking differences of binding were observed in the developing and adult heart, in which VEGF decorated all vessels, whereas strong VEGF-C signals were obtained only from epicardial vessels. In the lymph nodes, VEGF and VEGF-C showed distinct binding patterns in agreement with the differential location of their specific receptors. These results show that both VEGF-C and VEGF target embryonic blood vessels, whereas a more selective binding of VEGF-C occurs to its lymphatic vascular receptor in certain adult tissues. Our results suggest that VEGF and VEGF-C have both overlapping and distinct activities via their endothelial receptors. (+info)Placenta growth factor and vascular endothelial growth factor B and C expression in microvascular endothelial cells and pericytes. Implication in autocrine and paracrine regulation of angiogenesis. (6/512)
We have shown previously that vascular endothelial growth factor (VEGF) synthesized by the cellular constituents of small vessels per se, viz. endothelial cells and pericytes, participates in the hypoxia-driven proliferation of both cell types (Nomura, M., Yamagishi, S., Harada, S., Hayashi, Y., Yamashima, T., Yamashita, J., Yamamoto, H. (1995) J. Biol. Chem. 270, 28316-28324; Yamagishi, S., Yonekura, H., Yamamoto, Y., Fujimori, H., Sakurai, S., Tanaka, N., and Yamamoto, H. (1999) Lab. Invest. 79, 501-509). In this study, we examined the expression of the recently isolated VEGF gene family members (placenta growth factor (PlGF), VEGF-B, and VEGF-C) in human dermal microvascular endothelial cells and bovine retinal pericytes cultured under various oxygen tensions. Quantitative reverse transcription-polymerase chain reaction analyses demonstrated that the two cell types possess not only VEGF (VEGF-A) mRNA, but also VEGF-B, VEGF-C, and PlGF mRNAs. Among them, only VEGF-A mRNA was induced under hypoxia. Competitive reverse transcription-polymerase chain reaction showed that, under normoxic conditions, the rank order of mRNA content in endothelial cells was PlGF > VEGF-B > VEGF-C > VEGF-A and that mRNA coding for PlGF was expressed at >100-fold higher levels than VEGF-A mRNA. In pericytes, the rank order was VEGF-C > VEGF-A > VEGF-B > PlGF, and approximately 7-fold higher levels of VEGF-C mRNA compared with VEGF-A mRNA were noted in this cell type. Furthermore, antisense inhibition of PlGF protein production lowered the endothelial cell synthesis of DNA under hypoxic conditions. The results suggest that these VEGF family members may also take active parts in angiogenesis. (+info)Vascular endothelial growth factor-C (VEGF-C) and its receptors KDR and flt-4 are expressed in AIDS-associated Kaposi's sarcoma. (7/512)
Kaposi's sarcoma is characterized by clusters of spindle-shaped cells that are considered to be tumor cells and by prominent vasculature. Whereas spindle cells are most likely endothelial in origin, it remains controversial whether they are of lymphatic or blood vascular derivation. To test the hypothesis that the lymphangiogenesis factor vascular endothelial growth factor-C and its receptors, KDR and flt-4, are involved in the pathogenesis of Kaposi's sarcoma, we performed in situ hybridizations and immunofluorescent stainings on human immunodeficiency virus-associated Kaposi's sarcoma. Spindle-shaped tumor cells strongly expressed KDR and flt-4 mRNA. Immunofluorescent staining confirmed expression of the flt-4 receptor in Kaposi's sarcoma cells, and double labeling revealed its colocalization with the endothelial cell marker CD31. Vascular endothelial growth factor-C was strongly expressed in blood vessels associated with Kaposi's sarcoma. In vitro, human dermal microvascular endothelial cells also expressed vascular endothelial growth factor-C mRNA that was further upregulated by vascular permeability factor/vascular endothelial growth factor. Vascular endothelial growth factor-C potently stimulated the proliferation of Kaposi's sarcoma tumor cells in vitro. These results demonstrate important paracrine functions of vascular endothelial growth factor-C, produced by blood vessels, in the pathogenesis of cutaneous Kaposi's sarcoma, and suggest a lymphatic origin and/or differentiation of Kaposi's sarcoma tumor cells. (+info)High-level expression of angiogenic factors is associated with advanced tumor stage in human neuroblastomas. (8/512)
Angiogenesis is essential for tumor growth and metastasis and depends on the production of angiogenic factors by tumor cells. Neuroblastoma (NB) is a common pediatric tumor of neural crest origin, which is biologically and clinically heterogeneous. Increased tumor vascular index correlates with poor outcome of NB. To determine which angiogenic factors contribute to NB angiogenesis and thereby support tumor progression, we examined the expression of eight angiogenic factors [vascular endothelial growth factor (VEGF), VEGF-B, VEGF-C, basic fibroblast growth factor, angiopoietin (Ang)-1, Ang-2, transforming growth factor alpha, and platelet-derived growth factor (PDGF)] by semiquantitative RT-PCR in 37 NB primary tumors and in 22 NB cell lines. We also analyzed the relationship between angiogenic factor expression and clinicopathological factors as well as patient survival. All eight angiogenic factors examined were expressed at various levels in NB cell lines and tumors, suggesting their involvement in NB angiogenesis. The expression levels of most angiogenic factors were correlated with each other, suggesting their synergy in regulating the angiogenic process. Significantly higher expression levels of VEGF, VEGF-B, VEGF-C, basic fibroblast growth factor, Ang-2, transforming growth factor alpha, and PDGF-A (P < 0.0001-0.026) were found in advanced-stage tumors (stages 3 and 4) compared with low-stage tumors (stages 1, 2, and 4S). Expression of PDGF-A was significantly associated with patient survival (P = 0.04). The redundancy in angiogenic factor expression suggests that inhibition of VEGF bioactivity alone might not be a sufficient approach for antiangiogenic therapy of human NB. (+info)Vascular Endothelial Growth Factor C (VEGF-C) is a protein that belongs to the family of vascular endothelial growth factors. It plays a crucial role in angiogenesis, which is the formation of new blood vessels from pre-existing ones. Specifically, VEGF-C is a key regulator of lymphangiogenesis, which is the development of new lymphatic vessels.
VEGF-C stimulates the growth and proliferation of lymphatic endothelial cells, leading to an increase in the number and size of lymphatic vessels. This process is important for maintaining fluid balance in tissues and for the immune system's response to infection and inflammation.
Abnormal regulation of VEGF-C has been implicated in various diseases, including cancer, where it can promote tumor growth and metastasis by enhancing the formation of new blood vessels that supply nutrients and oxygen to the tumor. Inhibitors of VEGF-C have been developed as potential therapeutic agents for cancer treatment.
Vascular Endothelial Growth Factor Receptor-3 (VEGFR-3) is a type of receptor tyrosine kinase that is primarily expressed in lymphatic endothelial cells. It is a crucial regulator of lymphangiogenesis, which is the formation of new lymphatic vessels from pre-existing ones. VEGFR-3 binds to its ligands, including VEGF-C and VEGF-D, leading to the activation of downstream signaling pathways that promote cell survival, proliferation, migration, and differentiation of lymphatic endothelial cells.
VEGFR-3 also plays a role in angiogenesis, which is the formation of new blood vessels from pre-existing ones. However, its functions in angiogenesis are less well understood compared to its roles in lymphangiogenesis. Dysregulation of VEGFR-3 signaling has been implicated in various pathological conditions, including cancer, inflammation, and lymphatic disorders.
Lymphangiogenesis is the formation of new lymphatic vessels from pre-existing ones. It is a complex biological process that involves the growth, differentiation, and remodeling of lymphatic endothelial cells, which line the interior surface of lymphatic vessels. Lymphangiogenesis plays crucial roles in various physiological processes, including tissue drainage, immune surveillance, and lipid absorption. However, it can also contribute to pathological conditions such as cancer metastasis, inflammation, and fibrosis when it is dysregulated.
The process of lymphangiogenesis is regulated by a variety of growth factors, receptors, and signaling molecules, including vascular endothelial growth factor (VEGF)-C, VEGF-D, and their receptor VEGFR-3, as well as other factors such as angiopoietins, integrins, and matrix metalloproteinases. Understanding the mechanisms of lymphangiogenesis has important implications for developing novel therapies for a range of diseases associated with abnormal lymphatic vessel growth and function.
Lymphatic vessels are thin-walled, valved structures that collect and transport lymph, a fluid derived from the interstitial fluid surrounding the cells, throughout the lymphatic system. They play a crucial role in immune function and maintaining fluid balance in the body. The primary function of lymphatic vessels is to return excess interstitial fluid, proteins, waste products, and immune cells to the bloodstream via the subclavian veins near the heart.
There are two types of lymphatic vessels:
1. Lymphatic capillaries: These are the smallest lymphatic vessels, found in most body tissues except for the central nervous system (CNS). They have blind ends and are highly permeable to allow the entry of interstitial fluid, proteins, and other large molecules.
2. Larger lymphatic vessels: These include precollecting vessels, collecting vessels, and lymphatic trunks. Precollecting vessels have valves that prevent backflow of lymph and merge to form larger collecting vessels. Collecting vessels contain smooth muscle in their walls, which helps to propel the lymph forward. They also have valves at regular intervals to ensure unidirectional flow towards the heart. Lymphatic trunks are large vessels that collect lymph from various regions of the body and eventually drain into the two main lymphatic ducts: the thoracic duct and the right lymphatic duct.
Overall, lymphatic vessels play a vital role in maintaining fluid balance, immune surveillance, and waste removal in the human body.
Vascular Endothelial Growth Factor A (VEGFA) is a specific isoform of the vascular endothelial growth factor (VEGF) family. It is a well-characterized signaling protein that plays a crucial role in angiogenesis, the process of new blood vessel formation from pre-existing vessels. VEGFA stimulates the proliferation and migration of endothelial cells, which line the interior surface of blood vessels, thereby contributing to the growth and development of new vasculature. This protein is essential for physiological processes such as embryonic development and wound healing, but it has also been implicated in various pathological conditions, including cancer, age-related macular degeneration, and diabetic retinopathy. The regulation of VEGFA expression and activity is critical to maintaining proper vascular function and homeostasis.
Endothelial growth factors (ECGFs or EGFs) are a group of signaling proteins that stimulate the growth, proliferation, and survival of endothelial cells, which line the interior surface of blood vessels. These growth factors play crucial roles in various physiological processes, including angiogenesis (the formation of new blood vessels), wound healing, and vascular development during embryogenesis.
One of the most well-studied EGFs is the vascular endothelial growth factor (VEGF) family, which consists of several members like VEGFA, VEGFB, VEGFC, VEGFD, and placental growth factor (PlGF). These factors bind to specific receptors on the surface of endothelial cells, leading to a cascade of intracellular signaling events that ultimately result in cell proliferation, migration, and survival.
Other EGFs include fibroblast growth factors (FGFs), hepatocyte growth factor (HGF), platelet-derived growth factor (PDGF), and transforming growth factor-beta (TGF-β). Dysregulation of endothelial growth factors has been implicated in various pathological conditions, such as cancer, diabetic retinopathy, age-related macular degeneration, and cardiovascular diseases. Therefore, understanding the functions and regulation of EGFs is essential for developing novel therapeutic strategies to treat these disorders.
Vascular Endothelial Growth Factor D (VEGFD) is a protein that belongs to the family of vascular endothelial growth factors. It plays an essential role in the process of angiogenesis, which is the formation of new blood vessels from pre-existing ones. Specifically, VEGFD stimulates the growth and proliferation of lymphatic endothelial cells, thereby promoting the development and maintenance of the lymphatic system.
VEGFD binds to its specific receptor, VEGFR-3, which is primarily expressed on the surface of lymphatic endothelial cells. This binding triggers a cascade of intracellular signaling events that ultimately lead to the activation of various genes involved in cell proliferation, migration, and survival.
Dysregulation of VEGFD and its receptor has been implicated in several pathological conditions, including lymphatic malformations, cancer, and inflammatory diseases. In these contexts, the overexpression or aberrant activation of VEGFD can contribute to excessive angiogenesis and lymphangiogenesis, leading to tissue edema, tumor growth, and metastasis. Therefore, targeting the VEGFD signaling pathway has emerged as a promising therapeutic strategy for various diseases.
The lymphatic system is a complex network of organs, tissues, vessels, and cells that work together to defend the body against infectious diseases and also play a crucial role in the immune system. It is made up of:
1. Lymphoid Organs: These include the spleen, thymus, lymph nodes, tonsils, adenoids, and Peyer's patches (in the intestines). They produce and mature immune cells.
2. Lymphatic Vessels: These are thin tubes that carry clear fluid called lymph towards the heart.
3. Lymph: This is a clear-to-white fluid that contains white blood cells, mainly lymphocytes, which help fight infections.
4. Other tissues and cells: These include bone marrow where immune cells are produced, and lymphocytes (T cells and B cells) which are types of white blood cells that help protect the body from infection and disease.
The primary function of the lymphatic system is to transport lymph throughout the body, collecting waste products, bacteria, viruses, and other foreign substances from the tissues, and filtering them out through the lymph nodes. The lymphatic system also helps in the absorption of fats and fat-soluble vitamins from food in the digestive tract.
Vascular Endothelial Growth Factors (VEGFs) are a family of signaling proteins that stimulate the growth and development of new blood vessels, a process known as angiogenesis. They play crucial roles in both physiological and pathological conditions, such as embryonic development, wound healing, and tumor growth. Specifically, VEGFs bind to specific receptors on the surface of endothelial cells, which line the interior surface of blood vessels, triggering a cascade of intracellular signaling events that promote cell proliferation, migration, and survival. Dysregulation of VEGF signaling has been implicated in various diseases, including cancer, age-related macular degeneration, and diabetic retinopathy.
Lymphatic metastasis is the spread of cancer cells from a primary tumor to distant lymph nodes through the lymphatic system. It occurs when malignant cells break away from the original tumor, enter the lymphatic vessels, and travel to nearby or remote lymph nodes. Once there, these cancer cells can multiply and form new tumors, leading to further progression of the disease. Lymphatic metastasis is a common way for many types of cancer to spread and can have significant implications for prognosis and treatment strategies.
Vascular Endothelial Growth Factor Receptor-2 (VEGFR-2) is a tyrosine kinase receptor that is primarily expressed on vascular endothelial cells. It is a crucial regulator of angiogenesis, the process of new blood vessel formation from pre-existing vessels. VEGFR-2 is activated by binding to its ligand, Vascular Endothelial Growth Factor-A (VEGF-A), leading to receptor dimerization and autophosphorylation. This activation triggers a cascade of intracellular signaling events that promote endothelial cell proliferation, migration, survival, and vascular permeability, all essential steps in the angiogenic process.
VEGFR-2 plays a significant role in physiological and pathological conditions associated with angiogenesis, such as embryonic development, wound healing, tumor growth, and retinopathies. Inhibition of VEGFR-2 signaling has been an attractive target for anti-angiogenic therapies in various diseases, including cancer and age-related macular degeneration.
Vascular endothelial growth factor (VEGF) receptors are a type of cell surface receptor that play crucial roles in the process of angiogenesis, which is the formation of new blood vessels from pre-existing ones. These receptors bind to VEGF proteins, leading to a cascade of intracellular signaling events that ultimately result in the proliferation, migration, and survival of endothelial cells, which line the interior surface of blood vessels. There are three main types of VEGF receptors: VEGFR-1, VEGFR-2, and VEGFR-3. These receptors have distinct roles in angiogenesis, with VEGFR-2 being the primary mediator of this process. Dysregulation of VEGF signaling has been implicated in various diseases, including cancer, age-related macular degeneration, and diabetic retinopathy, making VEGF receptors important targets for therapeutic intervention.
Lymphokines are a type of cytokines that are produced and released by activated lymphocytes, a type of white blood cell, in response to an antigenic stimulation. They play a crucial role in the regulation of immune responses and inflammation. Lymphokines can mediate various biological activities such as chemotaxis, activation, proliferation, and differentiation of different immune cells including lymphocytes, monocytes, macrophages, and eosinophils. Examples of lymphokines include interleukins (ILs), interferons (IFNs), tumor necrosis factor (TNF), and colony-stimulating factors (CSFs).
Vascular Endothelial Growth Factor Receptor-1 (VEGFR-1), also known as Flt-1 (Fms-like tyrosine kinase-1), is a receptor tyrosine kinase that plays a crucial role in the regulation of angiogenesis, vasculogenesis, and lymphangiogenesis. It is primarily expressed on vascular endothelial cells, hematopoietic stem cells, and monocytes/macrophages. VEGFR-1 binds to several ligands, including Vascular Endothelial Growth Factor-A (VEGF-A), VEGF-B, and Placental Growth Factor (PlGF). The binding of these ligands to VEGFR-1 triggers intracellular signaling cascades that modulate various cellular responses, such as proliferation, migration, survival, and vascular permeability. While VEGFR-1 is known to have a role in promoting angiogenesis under certain conditions, it primarily acts as a negative regulator of angiogenesis by sequestering VEGF-A, preventing its binding to the more proangiogenic VEGFR-2 receptor. Dysregulation of VEGFR-1 signaling has been implicated in various pathological conditions, including cancer, inflammation, and vascular diseases.
Pathologic neovascularization is the abnormal growth of new blood vessels in previously avascular tissue or excessive growth within existing vasculature, which occurs as a result of hypoxia, inflammation, or angiogenic stimuli. These newly formed vessels are often disorganized, fragile, and lack proper vessel hierarchy, leading to impaired blood flow and increased vascular permeability. Pathologic neovascularization can be observed in various diseases such as cancer, diabetic retinopathy, age-related macular degeneration, and chronic inflammation. This process contributes to disease progression by promoting tumor growth, metastasis, and edema formation, ultimately leading to tissue damage and organ dysfunction.
Physiologic neovascularization is the natural and controlled formation of new blood vessels in the body, which occurs as a part of normal growth and development, as well as in response to tissue repair and wound healing. This process involves the activation of endothelial cells, which line the interior surface of blood vessels, and their migration, proliferation, and tube formation to create new capillaries. Physiologic neovascularization is tightly regulated by a balance of pro-angiogenic and anti-angiogenic factors, ensuring that it occurs only when and where it is needed. It plays crucial roles in various physiological processes, such as embryonic development, tissue regeneration, and wound healing.
Growth factor receptors are a type of cell surface receptor that bind to specific growth factors, which are signaling molecules that play crucial roles in regulating various cellular processes such as growth, differentiation, and survival. These receptors have an extracellular domain that can recognize and bind to the growth factor and an intracellular domain that can transduce the signal into the cell through a series of biochemical reactions.
There are several types of growth factors, including fibroblast growth factors (FGFs), epidermal growth factors (EGFs), vascular endothelial growth factors (VEGFs), and transforming growth factors (TGFs). Each type of growth factor has its own specific receptor or family of receptors.
Once a growth factor binds to its receptor, it triggers a cascade of intracellular signaling events that ultimately lead to changes in gene expression, protein synthesis, and other cellular responses. These responses can include the activation of enzymes, the regulation of ion channels, and the modulation of cytoskeletal dynamics.
Abnormalities in growth factor receptor signaling have been implicated in various diseases, including cancer, developmental disorders, and autoimmune diseases. For example, mutations in growth factor receptors can lead to uncontrolled cell growth and division, which is a hallmark of cancer. Therefore, understanding the structure and function of growth factor receptors has important implications for the development of new therapies for these diseases.
Angiogenesis inhibitors are a class of drugs that block the growth of new blood vessels (angiogenesis). They work by targeting specific molecules involved in the process of angiogenesis, such as vascular endothelial growth factor (VEGF) and its receptors. By blocking these molecules, angiogenesis inhibitors can prevent the development of new blood vessels that feed tumors, thereby slowing or stopping their growth.
Angiogenesis inhibitors are used in the treatment of various types of cancer, including colon, lung, breast, kidney, and ovarian cancer. They may be given alone or in combination with other cancer treatments, such as chemotherapy or radiation therapy. Some examples of angiogenesis inhibitors include bevacizumab (Avastin), sorafenib (Nexavar), sunitinib (Sutent), and pazopanib (Votrient).
It's important to note that while angiogenesis inhibitors can be effective in treating cancer, they can also have serious side effects, such as high blood pressure, bleeding, and damage to the heart or kidneys. Therefore, it's essential that patients receive careful monitoring and management of these potential side effects while undergoing treatment with angiogenesis inhibitors.
Immunohistochemistry (IHC) is a technique used in pathology and laboratory medicine to identify specific proteins or antigens in tissue sections. It combines the principles of immunology and histology to detect the presence and location of these target molecules within cells and tissues. This technique utilizes antibodies that are specific to the protein or antigen of interest, which are then tagged with a detection system such as a chromogen or fluorophore. The stained tissue sections can be examined under a microscope, allowing for the visualization and analysis of the distribution and expression patterns of the target molecule in the context of the tissue architecture. Immunohistochemistry is widely used in diagnostic pathology to help identify various diseases, including cancer, infectious diseases, and immune-mediated disorders.
Vascular Endothelial Growth Factor B (VEGFB) is a protein that belongs to the family of vascular endothelial growth factors. It is primarily involved in the regulation of angiogenesis, which is the formation of new blood vessels from pre-existing ones. VEGFB specifically stimulates the growth and survival of the endothelial cells that line the interior surface of blood vessels.
VEGFB plays a crucial role in the development and function of the cardiovascular system, as well as in various physiological processes such as wound healing and tissue repair. However, abnormal regulation of VEGFB has been implicated in several pathological conditions, including cancer, where it can contribute to tumor angiogenesis and metastasis, and diabetic retinopathy, where it can lead to the growth of new, leaky blood vessels in the eye.
It is important to note that while VEGFB has been extensively studied, there is still much to learn about its precise functions and regulatory mechanisms, and ongoing research continues to shed light on its role in health and disease.
Receptor Protein-Tyrosine Kinases (RTKs) are a type of transmembrane receptors found on the cell surface that play a crucial role in signal transduction and regulation of various cellular processes, including cell growth, differentiation, metabolism, and survival. They are called "tyrosine kinases" because they possess an intrinsic enzymatic activity that catalyzes the transfer of a phosphate group from ATP to tyrosine residues on target proteins, thereby modulating their function.
RTKs are composed of three main domains: an extracellular domain that binds to specific ligands (growth factors, hormones, or cytokines), a transmembrane domain that spans the cell membrane, and an intracellular domain with tyrosine kinase activity. Upon ligand binding, RTKs undergo conformational changes that lead to their dimerization or oligomerization, which in turn activates their tyrosine kinase activity. Activated RTKs then phosphorylate specific tyrosine residues on downstream signaling proteins, initiating a cascade of intracellular signaling events that ultimately result in the appropriate cellular response.
Dysregulation of RTK signaling has been implicated in various human diseases, including cancer, diabetes, and developmental disorders. As such, RTKs are important targets for therapeutic intervention in these conditions.
Fibroblast Growth Factor 2 (FGF-2), also known as basic fibroblast growth factor, is a protein involved in various biological processes such as cell growth, proliferation, and differentiation. It plays a crucial role in wound healing, embryonic development, and angiogenesis (the formation of new blood vessels). FGF-2 is produced and secreted by various cells, including fibroblasts, and exerts its effects by binding to specific receptors on the cell surface, leading to activation of intracellular signaling pathways. It has been implicated in several diseases, including cancer, where it can contribute to tumor growth and progression.
The endothelium is a thin layer of simple squamous epithelial cells that lines the interior surface of blood vessels, lymphatic vessels, and heart chambers. The vascular endothelium, specifically, refers to the endothelial cells that line the blood vessels. These cells play a crucial role in maintaining vascular homeostasis by regulating vasomotor tone, coagulation, platelet activation, inflammation, and permeability of the vessel wall. They also contribute to the growth and repair of the vascular system and are involved in various pathological processes such as atherosclerosis, hypertension, and diabetes.
Endothelial cells are the type of cells that line the inner surface of blood vessels, lymphatic vessels, and heart chambers. They play a crucial role in maintaining vascular homeostasis by controlling vasomotor tone, coagulation, platelet activation, and inflammation. Endothelial cells also regulate the transport of molecules between the blood and surrounding tissues, and contribute to the maintenance of the structural integrity of the vasculature. They are flat, elongated cells with a unique morphology that allows them to form a continuous, nonthrombogenic lining inside the vessels. Endothelial cells can be isolated from various tissues and cultured in vitro for research purposes.
Messenger RNA (mRNA) is a type of RNA (ribonucleic acid) that carries genetic information copied from DNA in the form of a series of three-base code "words," each of which specifies a particular amino acid. This information is used by the cell's machinery to construct proteins, a process known as translation. After being transcribed from DNA, mRNA travels out of the nucleus to the ribosomes in the cytoplasm where protein synthesis occurs. Once the protein has been synthesized, the mRNA may be degraded and recycled. Post-transcriptional modifications can also occur to mRNA, such as alternative splicing and addition of a 5' cap and a poly(A) tail, which can affect its stability, localization, and translation efficiency.
"Cells, cultured" is a medical term that refers to cells that have been removed from an organism and grown in controlled laboratory conditions outside of the body. This process is called cell culture and it allows scientists to study cells in a more controlled and accessible environment than they would have inside the body. Cultured cells can be derived from a variety of sources, including tissues, organs, or fluids from humans, animals, or cell lines that have been previously established in the laboratory.
Cell culture involves several steps, including isolation of the cells from the tissue, purification and characterization of the cells, and maintenance of the cells in appropriate growth conditions. The cells are typically grown in specialized media that contain nutrients, growth factors, and other components necessary for their survival and proliferation. Cultured cells can be used for a variety of purposes, including basic research, drug development and testing, and production of biological products such as vaccines and gene therapies.
It is important to note that cultured cells may behave differently than they do in the body, and results obtained from cell culture studies may not always translate directly to human physiology or disease. Therefore, it is essential to validate findings from cell culture experiments using additional models and ultimately in clinical trials involving human subjects.
Hypoxia-Inducible Factor 1 (HIF-1) is a transcription factor that plays a crucial role in the body's response to low oxygen levels, also known as hypoxia. HIF-1 is a heterodimeric protein composed of two subunits: an alpha subunit (HIF-1α) and a beta subunit (HIF-1β).
The alpha subunit, HIF-1α, is the regulatory subunit that is subject to oxygen-dependent degradation. Under normal oxygen conditions (normoxia), HIF-1α is constantly produced in the cell but is rapidly degraded by proteasomes due to hydroxylation of specific proline residues by prolyl hydroxylase domain-containing proteins (PHDs). This hydroxylation reaction requires oxygen as a substrate, and under hypoxic conditions, the activity of PHDs is inhibited, leading to the stabilization and accumulation of HIF-1α.
Once stabilized, HIF-1α translocates to the nucleus, where it heterodimerizes with HIF-1β and binds to hypoxia-responsive elements (HREs) in the promoter regions of target genes. This binding results in the activation of gene transcription programs that promote cellular adaptation to low oxygen levels. These adaptive responses include increased erythropoiesis, angiogenesis, glucose metabolism, and pH regulation, among others.
Therefore, HIF-1α is a critical regulator of the body's response to hypoxia, and its dysregulation has been implicated in various pathological conditions, including cancer, cardiovascular disease, and neurodegenerative disorders.
Replication Protein C (RPC or RFC) is not a single protein but a complex of five different proteins, which are essential for the process of DNA replication in eukaryotic cells. The individual subunits of the RPC complex are designated as RFC1, RFC2, RFC3, RFC4, and RFC5.
The primary function of the RPC complex is to load the clamp protein, proliferating cell nuclear antigen (PCNA), onto DNA at the primer-template junction during DNA replication. PCNA acts as a sliding clamp that encircles the DNA duplex and tethers the DNA polymerase to the template, thereby increasing its processivity.
RPC also plays a role in various other cellular processes, including nucleotide excision repair, DNA damage bypass, and checkpoint control during DNA replication. Defects in RPC have been linked to several human genetic disorders, such as cerebro-oculo-facio-skeletal syndrome (COFS) and xeroderma pigmentosum complementation group E (XP-E).
Neuropilin-1 (NRP-1) is a cell surface glycoprotein receptor that has been identified as having roles in both nervous system development and cancer biology. It was initially described as a receptor for semaphorins, which are guidance cues involved in axon pathfinding during neuronal development. However, it is now known to also function as a co-receptor for vascular endothelial growth factor (VEGF), playing critical roles in angiogenesis and lymphangiogenesis.
NRP-1 contains several distinct domains that allow it to interact with various ligands and coreceptors, including a extracellular domain containing two complement-binding protein-like domains, a membrane-proximal MAM (meprin A5, reversion-inducing cysteine-rich protein, and KAZAL) domain, and an intracellular domain.
In cancer biology, NRP-1 has been found to be overexpressed in many tumor types, where it contributes to tumor growth, progression, and metastasis by promoting angiogenesis, lymphangiogenesis, and tumor cell survival, migration, and invasion. Therefore, NRP-1 is considered a promising therapeutic target for cancer treatment.
Intercellular signaling peptides and proteins are molecules that mediate communication and interaction between different cells in living organisms. They play crucial roles in various biological processes, including cell growth, differentiation, migration, and apoptosis (programmed cell death). These signals can be released into the extracellular space, where they bind to specific receptors on the target cell's surface, triggering intracellular signaling cascades that ultimately lead to a response.
Peptides are short chains of amino acids, while proteins are larger molecules made up of one or more polypeptide chains. Both can function as intercellular signaling molecules by acting as ligands for cell surface receptors or by being cleaved from larger precursor proteins and released into the extracellular space. Examples of intercellular signaling peptides and proteins include growth factors, cytokines, chemokines, hormones, neurotransmitters, and their respective receptors.
These molecules contribute to maintaining homeostasis within an organism by coordinating cellular activities across tissues and organs. Dysregulation of intercellular signaling pathways has been implicated in various diseases, such as cancer, autoimmune disorders, and neurodegenerative conditions. Therefore, understanding the mechanisms underlying intercellular signaling is essential for developing targeted therapies to treat these disorders.
Angiogenesis inducing agents are substances or drugs that stimulate the growth of new blood vessels, a process known as angiogenesis. This process is essential for the growth and development of tissues and organs in the body, including wound healing and the formation of blood vessels in the placenta during pregnancy. However, abnormal angiogenesis can also contribute to various diseases, such as cancer, diabetic retinopathy, and age-related macular degeneration.
Angiogenesis inducing agents are being studied for their potential therapeutic benefits in a variety of medical conditions. For example, they may be used to promote wound healing or tissue repair after injury or surgery. In cancer treatment, angiogenesis inhibitors are often used to block the growth of new blood vessels and prevent tumors from growing and spreading. However, angiogenesis inducing agents can have the opposite effect and may potentially be used to enhance the delivery of drugs to tumors or improve the effectiveness of other cancer treatments.
Examples of angiogenesis inducing agents include certain growth factors, such as vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), and platelet-derived growth factor (PDGF). These substances can be administered as drugs to stimulate angiogenesis in specific contexts. Other substances, such as hypoxia-inducible factors (HIFs) and prostaglandins, can also induce angiogenesis under certain conditions.
Signal transduction is the process by which a cell converts an extracellular signal, such as a hormone or neurotransmitter, into an intracellular response. This involves a series of molecular events that transmit the signal from the cell surface to the interior of the cell, ultimately resulting in changes in gene expression, protein activity, or metabolism.
The process typically begins with the binding of the extracellular signal to a receptor located on the cell membrane. This binding event activates the receptor, which then triggers a cascade of intracellular signaling molecules, such as second messengers, protein kinases, and ion channels. These molecules amplify and propagate the signal, ultimately leading to the activation or inhibition of specific cellular responses.
Signal transduction pathways are highly regulated and can be modulated by various factors, including other signaling molecules, post-translational modifications, and feedback mechanisms. Dysregulation of these pathways has been implicated in a variety of diseases, including cancer, diabetes, and neurological disorders.
Angiopoietin-1 (ANG-1) is a protein that plays a crucial role in the development and maintenance of blood vessels. It is a member of the angiopoietin family, which includes several growth factors involved in the regulation of angiogenesis, the formation of new blood vessels from pre-existing ones.
ANG-1 primarily binds to the Tie2 receptor, which is predominantly expressed on vascular endothelial cells. The ANG-1/Tie2 signaling pathway promotes vascular stability, integrity, and maturation by enhancing endothelial cell survival, migration, and adhesion. It also inhibits vascular leakage and inflammation, contributing to the overall homeostasis of the vasculature.
In addition to its role in physiological conditions, ANG-1 has been implicated in various pathological processes such as tumor angiogenesis, ischemia, and fibrosis. Modulation of the ANG-1/Tie2 signaling pathway has emerged as a potential therapeutic strategy for treating several diseases associated with abnormal vascular function.
Epidermal Growth Factor (EGF) is a small polypeptide that plays a significant role in various biological processes, including cell growth, proliferation, differentiation, and survival. It primarily binds to the Epidermal Growth Factor Receptor (EGFR) on the surface of target cells, leading to the activation of intracellular signaling pathways that regulate these functions.
EGF is naturally produced in various tissues, such as the skin, and is involved in wound healing, tissue regeneration, and maintaining the integrity of epithelial tissues. In addition to its physiological roles, EGF has been implicated in several pathological conditions, including cancer, where it can contribute to tumor growth and progression by promoting cell proliferation and survival.
As a result, EGF and its signaling pathways have become targets for therapeutic interventions in various diseases, particularly cancer. Inhibitors of EGFR or downstream signaling components are used in the treatment of several types of malignancies, such as non-small cell lung cancer, colorectal cancer, and head and neck cancer.
"Nude mice" is a term used in the field of laboratory research to describe a strain of mice that have been genetically engineered to lack a functional immune system. Specifically, nude mice lack a thymus gland and have a mutation in the FOXN1 gene, which results in a failure to develop a mature T-cell population. This means that they are unable to mount an effective immune response against foreign substances or organisms.
The name "nude" refers to the fact that these mice also have a lack of functional hair follicles, resulting in a hairless or partially hairless phenotype. This feature is actually a secondary consequence of the same genetic mutation that causes their immune deficiency.
Nude mice are commonly used in research because their weakened immune system makes them an ideal host for transplanted tumors, tissues, and cells from other species, including humans. This allows researchers to study the behavior of these foreign substances in a living organism without the complication of an immune response. However, it's important to note that because nude mice lack a functional immune system, they must be kept in sterile conditions and are more susceptible to infection than normal mice.
Angiopoietin-2 (Ang-2) is a protein that is involved in the regulation of blood vessel formation and maintenance. It is a member of the angiopoietin family, which includes Ang-1, Ang-2, Ang-3, and Ang-4. These proteins bind to the Tie receptor tyrosine kinases (Tie1 and Tie2) on the surface of endothelial cells, which line the interior of blood vessels.
Ang-2 is primarily produced by endothelial cells and has context-dependent roles in angiogenesis, which is the growth of new blood vessels from pre-existing ones. In general, Ang-2 is thought to act as an antagonist of Ang-1, which promotes vessel stability and maturation.
Ang-2 can destabilize existing blood vessels by binding to Tie2 receptors and blocking the stabilizing effects of Ang-1. This can lead to increased vascular permeability and inflammation. However, in the presence of pro-angiogenic factors such as VEGF (vascular endothelial growth factor), Ang-2 can also promote the formation of new blood vessels by stimulating endothelial cell migration and proliferation.
Abnormal regulation of Ang-2 has been implicated in various diseases, including cancer, diabetic retinopathy, and age-related macular degeneration. In these conditions, increased levels of Ang-2 can contribute to the development of abnormal blood vessels, which can lead to tissue damage and loss of function.
Cell proliferation is the process by which cells increase in number, typically through the process of cell division. In the context of biology and medicine, it refers to the reproduction of cells that makes up living tissue, allowing growth, maintenance, and repair. It involves several stages including the transition from a phase of quiescence (G0 phase) to an active phase (G1 phase), DNA replication in the S phase, and mitosis or M phase, where the cell divides into two daughter cells.
Abnormal or uncontrolled cell proliferation is a characteristic feature of many diseases, including cancer, where deregulated cell cycle control leads to excessive and unregulated growth of cells, forming tumors that can invade surrounding tissues and metastasize to distant sites in the body.
Rosacea is a chronic skin condition primarily characterized by persistent redness, inflammation, and visible blood vessels on the face, particularly the nose, cheeks, forehead, and chin. It can also cause small, red, pus-filled bumps. Rosacea typically affects adults between 30 and 50 years old, with fair skin types being more susceptible. The exact cause of rosacea is unknown, but it's believed to be a combination of genetic and environmental factors, including abnormal facial blood vessels, immune system issues, and certain triggers (such as sun exposure, emotional stress, hot or cold weather, heavy exercise, alcohol consumption, spicy foods, and certain skin care products). There is no cure for rosacea, but various treatments can help control its symptoms and improve the appearance of the skin. These may include topical medications, oral antibiotics, laser therapy, and lifestyle modifications to avoid triggers.
Erythema is a term used in medicine to describe redness of the skin, which occurs as a result of increased blood flow in the superficial capillaries. This redness can be caused by various factors such as inflammation, infection, trauma, or exposure to heat, cold, or ultraviolet radiation. In some cases, erythema may also be accompanied by other symptoms such as swelling, warmth, pain, or itching. It is a common finding in many medical conditions and can vary in severity from mild to severe.
Facial dermatoses refer to various skin conditions that affect the face. These can include a wide range of disorders, such as:
1. Acne vulgaris: A common skin condition characterized by the formation of comedones (blackheads and whiteheads) and inflammatory papules, pustules, and nodules. It primarily affects the face, neck, chest, and back.
2. Rosacea: A chronic skin condition that causes redness, flushing, and visible blood vessels on the face, along with bumps or pimples and sometimes eye irritation.
3. Seborrheic dermatitis: A common inflammatory skin disorder that causes a red, itchy, and flaky rash, often on the scalp, face, and eyebrows. It can also affect other oily areas of the body, like the sides of the nose and behind the ears.
4. Atopic dermatitis (eczema): A chronic inflammatory skin condition that causes red, itchy, and scaly patches on the skin. While it can occur anywhere on the body, it frequently affects the face, especially in infants and young children.
5. Psoriasis: An autoimmune disorder that results in thick, scaly, silvery, or red patches on the skin. It can affect any part of the body, including the face.
6. Contact dermatitis: A skin reaction caused by direct contact with an allergen or irritant, resulting in redness, itching, and inflammation. The face can be affected when allergens or irritants come into contact with the skin through cosmetics, skincare products, or other substances.
7. Lupus erythematosus: An autoimmune disorder that can cause a butterfly-shaped rash on the cheeks and nose, along with other symptoms like joint pain, fatigue, and photosensitivity.
8. Perioral dermatitis: A inflammatory skin condition that causes redness, small bumps, and dryness around the mouth, often mistaken for acne. It can also affect the skin around the nose and eyes.
9. Vitiligo: An autoimmune disorder that results in the loss of pigmentation in patches of skin, which can occur on the face and other parts of the body.
10. Tinea faciei: A fungal infection that affects the facial skin, causing red, scaly, or itchy patches. It is also known as ringworm of the face.
These are just a few examples of skin conditions that can affect the face. If you experience any unusual symptoms or changes in your skin, it's essential to consult a dermatologist for proper diagnosis and treatment.
Telangiectasia is a medical term that refers to the dilation and widening of small blood vessels called capillaries, leading to their visibility under the skin or mucous membranes. These dilated vessels often appear as tiny red lines or patterns, measuring less than 1 millimeter in diameter.
Telangiectasias can occur in various parts of the body, such as the face, nose, cheeks, legs, and fingers. They are typically harmless but may cause cosmetic concerns for some individuals. In certain cases, telangiectasias can be a sign of an underlying medical condition, like rosacea, hereditary hemorrhagic telangiectasia (HHT), or liver disease.
It is essential to consult with a healthcare professional if you notice any unusual changes in your skin or mucous membranes, as they can provide appropriate evaluation and treatment recommendations based on the underlying cause of the telangiectasias.
A "drug eruption" is a general term used to describe an adverse skin reaction that occurs as a result of taking a medication. These reactions can vary in severity and appearance, and may include symptoms such as rash, hives, itching, redness, blistering, or peeling of the skin. In some cases, drug eruptions can also cause systemic symptoms such as fever, fatigue, or joint pain.
The exact mechanism by which drugs cause eruptions is not fully understood, but it is thought to involve an abnormal immune response to the medication. There are many different types of drug eruptions, including morphilliform rashes, urticaria (hives), fixed drug eruptions, and Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN), which is a severe and potentially life-threatening reaction.
If you suspect that you are experiencing a drug eruption, it is important to seek medical attention promptly. Your healthcare provider can help determine the cause of the reaction and recommend appropriate treatment. In some cases, it may be necessary to discontinue the medication causing the reaction and switch to an alternative therapy.
Dermatologic agents are medications, chemicals, or other substances that are applied to the skin (dermis) for therapeutic or cosmetic purposes. They can be used to treat various skin conditions such as acne, eczema, psoriasis, fungal infections, and wounds. Dermatologic agents include topical corticosteroids, antibiotics, antifungals, retinoids, benzoyl peroxide, salicylic acid, and many others. They can come in various forms such as creams, ointments, gels, lotions, solutions, and patches. It is important to follow the instructions for use carefully to ensure safety and effectiveness.
Mite infestations refer to the presence and multiplication of mites, which are tiny arthropods belonging to the class Arachnida, on or inside a host's body. This can occur in various sites such as the skin, lungs, or gastrointestinal tract, depending on the specific mite species.
Skin infestations by mites, also known as dermatophilosis or mange, are common and may cause conditions like scabies (caused by Sarcoptes scabiei) or demodecosis (caused by Demodex spp.). These conditions can lead to symptoms such as itching, rash, and skin lesions.
Lung infestations by mites, although rare, can occur in people who work in close contact with mites, such as farmers or laboratory workers. This condition is called "mite lung" or "farmer's lung," which is often caused by exposure to high levels of dust containing mite feces and dead mites.
Gastrointestinal infestations by mites can occur in animals but are extremely rare in humans. The most common example is the intestinal roundworm, which belongs to the phylum Nematoda rather than Arachnida.
It's important to note that mite infestations can be treated with appropriate medical interventions and prevention measures.
Vascular endothelial growth factor
Vascular endothelial growth factor C
Vascular endothelial growth factor B
Vascular endothelial growth factor A
Vascular endothelial growth factor (VEGF) IRES A
Decoy
Therapeutic angiogenesis
Neutron capture therapy of cancer
Diabetic retinopathy
VEGFR1
FLT4
Cambiogenplasmid
Neuropilin 2
Glaucoma
Pachydermoperiostosis
Anti-VEGF
Secondary glaucoma
Mitogen
Autocrine signaling
RNA therapeutics
Molecular processor
Retinopathy
Malignant pleural effusion
Angiogenesis inhibitor
Bevacizumab
Gene therapy of the human retina
List of Italian inventions and discoveries
Aflibercept
Remitting seronegative symmetrical synovitis with pitting edema
Judah Folkman
Vascular endothelial growth factor C - Wikipedia
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VEGF53
- Vascular endothelial growth factor (VEGF, /vɛdʒˈɛf/), originally known as vascular permeability factor (VPF), is a signal protein produced by many cells that stimulates the formation of blood vessels. (wikipedia.org)
- To be specific, VEGF is a sub-family of growth factors, the platelet-derived growth factor family of cystine-knot growth factors. (wikipedia.org)
- Overexpression of VEGF can cause vascular disease in the retina of the eye and other parts of the body. (wikipedia.org)
- In 1989 Ferrara and Henzel described an identical factor in bovine pituitary follicular cells which they purified, cloned and named VEGF. (wikipedia.org)
- Activity of VEGF-A, as its name implies, has been studied mostly on cells of the vascular endothelium, although it does have effects on a number of other cell types (e.g., stimulation monocyte/macrophage migration, neurons, cancer cells, kidney epithelial cells). (wikipedia.org)
- In vitro, VEGF-A has been shown to stimulate endothelial cell mitogenesis and cell migration. (wikipedia.org)
- VEGF-A is also a vasodilator and increases microvascular permeability and was originally referred to as vascular permeability factor. (wikipedia.org)
- Vascular endothelial growth factor (VEGF), an established angiogenesis factor, is expressed in allografts undergoing rejection, but its function in the rejection process has not been defined. (jci.org)
- In vitro, we found that VEGF enhanced endothelial cell expression of the chemokines monocyte chemoattractant protein 1 and IL-8, and in combination with IFN-γ synergistically induced endothelial cell production of the potent T cell chemoattractant IFN-inducible protein-10 (IP-10). (jci.org)
- Anti-VEGF failed to inhibit T cell activation responses in vivo, but inhibited intragraft expression of several endothelial cell adhesion molecules and chemokines, including IP-10. (jci.org)
- We have previously demonstrated that a failure of pulmonary endothelial cell survival induced by vascular endothelial growth factor (VEGF) receptor blockade results in lung alveolar septal cell apoptosis and emphysema. (nih.gov)
- Vascular endothelial growth factor (VEGF) is an essential angiogenic factor for formation of the embryonic vasculature, and also has important roles in pathological conditions such as diabetic retinopthy, rheumatoid arthritis and cancer. (figshare.com)
- Two main VEGF receptors are expressed in endothelial cells: VEGFR-1 and VEGFR-2. (figshare.com)
- Patterns of expression of vascular endothelial growth factor (VEGF) and VEGF receptors in mice suggest a role in hormonally regulated angiogenesis. (jci.org)
- Vascular endothelial growth factor (VEGF) is a secreted endothelial cell-specific mitogen. (jci.org)
- VEGF-binding activity, on the other hand, was found on endothelial cells of both quiescent and proliferating blood vessels. (jci.org)
- We propose that excessive expression of VEGF during gonadotropin-induced ovulation may contribute to the development of ovarian hyperstimulation syndromes by virtue of the vascular permeabilization activity of this factor. (jci.org)
- 2005). The vascular endothelial growth factor (VEGF) is a 46 kD dimeric glycoprotein secreted by neoplastic cells, macrophages, plasma cells and lymphocytes, which triggers endothelial cell proliferation by interacting with specific receptors in a paracrine or autocrine fashion (Ferrara 2004). (vin.com)
- To measure intravitreal low-density lipoprotein receptor-related protein 6 (LRP6) and vascular endothelial growth factor (VEGF) levels in the eyes of patients with proliferative diabetic retinopathy (PDR) and to observe their correlation with PDR activity. (molvis.org)
- In this study, we explore the role of HMGB1 in advanced glycation end products (AGEs)-induced vascular endothelial growth factor A (VEGF-A) production in rat retinal ganglion cell line 5 (RGC-5) cells. (molvis.org)
- Objectives Vascular endothelial growth factor (VEGF) regulates vascular endothelial cell differentiation and angiogenesis, and maturation of epithelial cells of the developing lungs. (bmj.com)
- Different reports have described the role of VEGF in lung cells proliferation, differentiation, growth and permeability. (bmj.com)
- In this study we focus on the immunoreactivity of the monoclonal antibody VEGF (C-1) in order to analyze its expression in two cell populations of regenerating mouse liver (hepatocytes and endothelial cells) after partial hepatectomy, and two transplanted hepatocarcinomas (ES2 and SS1K). (unlp.edu.ar)
- The results showed strongly immunopositivity reaction for VEGF either in hepatocytes or endothelial cells of mouse regenerating liver. (unlp.edu.ar)
- This assay has high sensitivity and excellent specificity for detection of Endocrine Gland Derived Vascular Endothelial Growth Factor (EG-VEGF). (uscnk.com)
- No significant cross-reactivity or interference between Endocrine Gland Derived Vascular Endothelial Growth Factor (EG-VEGF) and analogues was observed. (uscnk.com)
- Matrices listed below were spiked with certain level of recombinant Endocrine Gland Derived Vascular Endothelial Growth Factor (EG-VEGF) and the recovery rates were calculated by comparing the measured value to the expected amount of Endocrine Gland Derived Vascular Endothelial Growth Factor (EG-VEGF) in samples. (uscnk.com)
- Intra-assay Precision (Precision within an assay): 3 samples with low, middle and high level Endocrine Gland Derived Vascular Endothelial Growth Factor (EG-VEGF) were tested 20 times on one plate, respectively. (uscnk.com)
- Inter-assay Precision (Precision between assays): 3 samples with low, middle and high level Endocrine Gland Derived Vascular Endothelial Growth Factor (EG-VEGF) were tested on 3 different plates, 8 replicates in each plate. (uscnk.com)
- The linearity of the kit was assayed by testing samples spiked with appropriate concentration of Endocrine Gland Derived Vascular Endothelial Growth Factor (EG-VEGF) and their serial dilutions. (uscnk.com)
- The microtiter plate provided in this kit has been pre-coated with an antibody specific to Endocrine Gland Derived Vascular Endothelial Growth Factor (EG-VEGF). (uscnk.com)
- Standards or samples are then added to the appropriate microtiter plate wells with a biotin-conjugated antibody specific to Endocrine Gland Derived Vascular Endothelial Growth Factor (EG-VEGF). (uscnk.com)
- The role of vascular endothelial growth factor (VEGF) in differential vWF expression was investigated using cultured human umbilical vein endothelial cells (HUVECs). (biomedcentral.com)
- In our fourth study, we discovered that VEGF-C, the ligand for VEGFR-2 and VEGFR-3, which has been known to be a major lymphangiogenic factor now reveals its a unique role in embryonic erythropoiesis but not in adults. (helsinki.fi)
- VEGF is a polypeptide structurally related to platelet-derived growth factor (PDGF). (definithing.com)
- Disclaimer: Vascular endothelial growth factor (VEGF) definition / meaning should not be considered complete, up to date, and is not intended to be used in place of a visit, consultation, or advice of a legal, medical, or any other professional. (definithing.com)
- During angiogenesis, a highly regulated process, the most potent pro-angiogenic signaling cascades are initiated by vascular endothelial growth factor (VEGF) binding to EC-resident VEGF receptors (VEGFR) like VEGFR1, VEGFR2 and VEGFR3 [ 9 ]. (biomedcentral.com)
- The loss of myoferlin results in lack of proliferation, migration, and nitric oxide (NO) release in response to vascular endothelial growth factor (VEGF). (elsevierpure.com)
- VEGFR-1, also called Flt-1, is the exclusive VEGFR present on the surface of monocytes and mediates a chemotactic response to VEGF-A and tissue factor induction. (cusabio.com)
- Can the vascular endothelial growth factor (VEGF) and total estradiol 17β be used as a marker of equine oocyte maturation? (cloud-clone.com)
- In cultured cells, the overexpression of Spred-1 or Spred-2 strongly suppressed vascular endothelial growth factor-C (VEGF-C)/VEGF receptor (VEGFR)-3-mediated ERK activation, while Spred-1/2-deficient cells were extremely sensitive to VEGFR-3 signaling. (elsevierpure.com)
- The aim of this study is to evaluate CD4(+), CD8(+), and CD45RO(+) T cells , and vascular endothelial growth factor ( VEGF ) expression in cyclosporin A (CsA)-induced rat overgrown gingival tissue during an 8-week period. (bvsalud.org)
- Vascular endothelial growth factor (VEGF) is a key stimulator of physiological and pathological angiogenesis. (ox.ac.uk)
- VEGF signals primarily through VEGF receptor 2 (VEGFR2), a receptor tyrosine kinase whose expression is found predominantly on endothelial cells. (ox.ac.uk)
- Our data suggest that a subset of NSCLC tumour cells express functional VEGFR2 which can act to promote VEGF-dependent tumour cell growth. (ox.ac.uk)
- Vascular endothelial growth factor (VEGF) plays a significant role in both physiologic and pathologic angiogenesis and plays a part in improved permeability across both blood-retinal and blood-brain barriers. (molecularcircuit.com)
- The vascular endothelial growth factor (VEGF) shows a positive effect on enhancing angiogenesis in vivo. (researcher.life)
- We investigated the influence of alpha6beta1 on vascular endothelial growth factor (VEGF) expression because autocrine VEGF is necessary for the survival of serum-deprived cells in hypoxia. (umassmed.edu)
- Background Vascular endothelial growth factor (VEGF) is produced by bladder cancer cell lines in vitro and expressed in human bladder tumor tissues. (johnshopkins.edu)
- Quantitative RT-PCR was used to asses mRNA levels of collagenase-1 (MMP-1), stromelysin (MMP-3), vascular endothelial growth factor (VEGF), connective tissue growth factor (CTGF), cyclooxygenase-2 (COX-2), interleukin-1β (IL-1β), type III collagen (COL-III) and fibronectin (FBRN). (cdc.gov)
- treatment options include intravitreal anti-vascular endothelial growth factor (anti-VEGF) injections or photodynamic therapy (PDT). (cdc.gov)
- ABSTRACT Allergic contact dermatitis to cement is a delayed-type hypersensitivity reaction in which cytokines interferon-gamma (IFN-) and vascular endothelial growth factor (VEGF) may be involved in persisting erythema and oedema. (who.int)
- VEGF pour vascular endothelial growth factor) peuvent être impliqués dans des érythèmes ou des oedèmes persistants. (who.int)
Receptors4
- The molecular mechanism by which vascular endothelial receptors (VEGFRs) control vessel growth and function in physiological and pathological settings is under intensive study, but questions remain. (helsinki.fi)
- Our third study showed that when all VEGFRs receptors are deleted, the organ-specificity and -sensitivity differ in different vascular beds. (helsinki.fi)
- Like other TNF-family receptors and the IL-1 receptor, RANK mediates its signal transduction via TNF receptor-associated factor (TRAF) proteins, suggesting that the signaling pathways activated by RANK and other inflammatory cytokines involved in osteoclast differentiation and activation are interconnected. (umassmed.edu)
- To understand the functional interactions between the TrkA and p75 nerve growth factor (NGF) receptors, we stably transfected LAN5 neuroblastoma cells with an expression vector for ET-R, a chimeric receptor with the extracellular domain of the epidermal growth factor receptor (EGFR), and the TrkA transmembrane and intracellular domains. (umassmed.edu)
Cells22
- We also demonstrated positive immunoreaction in both malignant tumors ES2 and SS1K endothelial and parenchymal cells. (unlp.edu.ar)
- Promotes proliferation, survival, migration and differentiation of endothelial cells. (drugbank.com)
- Required for VEGFA-mediated induction of NOS2 and NOS3, leading to the production of the signaling molecule nitric oxide (NO) by endothelial cells. (drugbank.com)
- vWF is produced exclusively by endothelial cells and megakaryocytes. (biomedcentral.com)
- Then, based on our earlier published findings, we further elucidate the role of VEGFR-3 in blood endothelial cells, using principally a genetic approach. (helsinki.fi)
- Adhesion experiment in vitro was performed with mouse microvascular endothelial cells (bEnd.3) and the ratio of the number of UCA to that of cells at the same field was compared. (thno.org)
- A substance made by cells that stimulates new blood vessel formation, a mitogen for vascular endothelial (vessel lining) cells. (definithing.com)
- Objectives Transforming growth factor (TGF)-β regulates the function of vascular endothelial cells and may be involved in endothelial dysfunction. (iium.edu.my)
- The expression of phosphorylated Smad linker proteins were determined following TGF-β stimulation in the absence and presence of different serine/threonine kinase inhibitors in vascular endothelial cells. (iium.edu.my)
- These phosphorylations provide an opportunity to further understand a therapeutically targeted and very specific signalling pathway in vascular endothelial cells. (iium.edu.my)
- For cells, cell lines and tissues in culture till half confluency.Aplha, transcription related growth factors and stimulating factors or repressing nuclear factors are complex subunits of proteins involved in cell differentiation. (cellcycl.com)
- In vascular smooth muscle cells (SMCs), VEGFR-1 is inducibly expressed by vascular injury and participates in neointimal development. (cusabio.com)
- The number of LYVE-1-positive lymphatic vessels and lymphatic endothelial cells increased markedly in Spred-1/2-deficient embryos compared with WT embryos, while the number of blood vessels was not different. (elsevierpure.com)
- Immunohistochemical analysis of CD45RO+ T cells and vascular endothelial growth factor expression in cyclosporin A-induced rat gingival tissue. (bvsalud.org)
- We determine a comprehensive map of lineage-specific lncRNAs in human dermal lymphatic and blood vascular endothelial cells (LECs and BECs), combining RNA-Seq and CAGE-Seq. (nature.com)
- During development, the blood vascular system arises from endothelial cell progenitors that differentiate from mesodermal cells, mostly through the expression of the transcription factor (TF) ETV2. (nature.com)
- Activation of the VEGFA/VEGFR2 signaling and expression of blood vascular endothelial cell (BEC) markers, such as NRP1 and EphrinB2, further differentiate these precursor cells into BECs, which then form the hierarchical network of blood vessels 4 . (nature.com)
- Thereafter, a distinct subpopulation of endothelial cells lining the cardinal vein starts differentiating by expressing the TF PROX1, the master regulator of lymphatic endothelial cell (LEC) identity, via the TFs SOX18 and COUPTFII. (nature.com)
- This vertical growth phase represents a key event for the cell spread, since it allows the cells to migrate deeply in the dermis, in the lymphatics, and the bloodstream. (hindawi.com)
- In the case of melanoma, circulating cells may find a suitable microenvironment in the first draining lymph node, known as the sentinel lymph node, in other lymphnodes or in distant organs, leading to secondary tumor growth (Figure 1 ). (hindawi.com)
- Lymphangioleiomyomatosis (LAM) is an indolent, progressive growth of smooth muscle cells throughout the lungs, pulmonary blood vessels, lymphatics, and pleurae. (msdmanuals.com)
- Specifically, molecular interactions between cancer-associated fibroblasts, pericytes and endothelial cells are explored with a special focus on novel anti-cancer strategies. (lu.se)
Receptor tyrosi2
- Because another growth/trophic factor that signals via a receptor tyrosine kinase (brain derived neurotrophic factor) elicits a long-lasting facilitation of respiratory motor activity in the phrenic nerve, we tested the hypothesis that VEGFA-165 elicits similar phrenic motor facilitation (pMF). (jneurosci.org)
- Pazopanib is a vascular endothelial receptor tyrosine kinase inhibitor with anti-angiogenesis and anti-tumor activity in several preclinical models. (johnshopkins.edu)
Anti-vascular endoth4
- Purpose: To investigate 12-month treatment outcomes of anti-vascular endothelial growth factor therapy in eyes with typical exudative age-related macular degeneration with good baseline visual acuity. (kyobobook.co.kr)
- Patients were treated with anti-vascular endothelial growth factor monotherapy during the 12-month follow-up period. (kyobobook.co.kr)
- Results: Patients received an average of 4.4 ± 1.3 intravitreal anti-vascular endothelial growth factor injections. (kyobobook.co.kr)
- For people who have vision loss from POHS, injections into the eye with a treatment called anti-vascular endothelial growth factor can help. (cdc.gov)
Polymorphisms4
- do Espírito Santo GF, Galera BB, Duarte EC, Chen ES, Azis L, Damazo AS, Saba GT, de Sousa Gehrke F, Guerreiro da Silva IDC, Waisberg J. Prognostic significance of vascular endothelial growth factor polymorphisms in colorectal cancer patients. (wjgnet.com)
- Polymorphisms of Vascular Endothelial Growth Factor and Retinopathy of Prematurity. (cdc.gov)
- Evaluation of Factor V Leiden, Prothrombin G20210A, MTHFR C677T and MTHFR A1298C gene polymorphisms in retinopathy of prematurity in a Turkish cohort. (cdc.gov)
- Recent advances have been made in the of host factors, polymorphisms, and candidate genes associated characterization of the immune response to low-molecular- with occupational asthma may improve our understanding of weight agents. (cdc.gov)
Lymphatic endothelial cell1
- Ex vivo colony assay revealed that Spred-1/2 suppressed lymphatic endothelial cell proliferation and/or differentiation. (elsevierpure.com)
VEGFR21
- Ultrasound (US) molecular imaging by examining the expression of vascular endothelial growth factor receptor 2 (VEGFR2) on uterus vascular endothelium was applied to evaluate the endometrial receptivity. (thno.org)
Embryonic2
- They are important signaling proteins involved in both vasculogenesis (the de novo formation of the embryonic circulatory system) and angiogenesis (the growth of blood vessels from pre-existing vasculature). (wikipedia.org)
- Plays an essential role in the regulation of angiogenesis, vascular development, vascular permeability, and embryonic hematopoiesis. (drugbank.com)
VEGFA2
- Although vascular endothelial growth factor (VEGFA-165) is primarily known for its role in angiogenesis, it also plays important neurotrophic and neuroprotective roles for spinal motor neurons. (jneurosci.org)
- Vascular endothelial growth factor A (VEGFA) plays a critical angiogenic role in the endometrium of placentalia during preimplantation. (uzh.ch)
Tissues2
- Herein, using a proteomic analysis of endothelial cell (EC) caveolae/lipid raft microdomains we identified myoferlin in these domains and show that myoferlin is highly expressed in ECs and vascular tissues. (elsevierpure.com)
- The blood and lymphatic vascular systems are essential for the efficient transport of oxygen, nutrients, signaling molecules, and leukocytes to and from peripheral tissues, the removal of waste products, and the preservation of fluid homeostasis. (nature.com)
Proteins2
- Specificity Human Vascular Endothelial Growth Factor receptor 1 Human sVEGFR1 isoforms, possibly primate sVEGFR1 (untested), homology to mouse, rat, chicken sVEGFR1 proteins less than 80% across the immunogen used. (biosensis.com)
- Spred/Sprouty family proteins negatively regulate growth factor-induced ERK activation. (elsevierpure.com)
Stimulates1
- Vascular endothelial growth factor directly stimulates tumour cell proliferation in non-small cell lung cancer. (ox.ac.uk)
Phosphorylation1
- Phosphorylation of vascular endothelial growth factor receptor 2 (pVEGFR2) via PI3K/Akt signaling plays a key role in mediating cellular processes involved in repair, such as mitogenesis, angiogenesis, and vascular permeability. (biomedcentral.com)
Cell8
- Diabetes causes retinal microvasculopathy associated with pericyte cell death, microaneurysms, abnormal vascular permeability, and macular edema. (molvis.org)
- Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Human Vascular Endothelial Growth Factor D (VEGFD) in serum, plasma, tissue homogenates, cell lysates, cell culture supernates and other biological fluids. (fslregister.nl)
- Description: Enzyme-linked immunosorbent assay based on the Double-antibody Sandwich method for detection of Human Vascular Endothelial Growth Factor D (VEGFD) in samples from serum, plasma, tissue homogenates, cell lysates, cell culture supernates and other biological fluids with no significant corss-reactivity with analogues from other species. (fslregister.nl)
- Description: A sandwich quantitative ELISA assay kit for detection of Rat Vascular Endothelial Growth Factor D (VEGFD) in samples from serum, plasma, tissue homogenates, cell lysates, cell culture supernates or other biological fluids. (fslregister.nl)
- Changes in these and other oncogenes can disrupt cell growth control, ultimately leading to the uncontrolled growth of cancer. (medscape.com)
- H- ras was one of the oncogenes that first caught the attention of molecular biologists interested in cell signaling, cell growth control, and cancer. (medscape.com)
- It and the gene for the epidermal growth factor receptor ( EGFR ) are involved in cell signaling. (medscape.com)
- We believe that decisive treatment benefit can only be achieved by targeting distinct cell types and pathways that collectively sustain tumor growth. (lu.se)
Retinal2
- Currently available, intravitreal, corticosteroid-release devices offer surgical and in-office management of retinal vascular disease and posterior uveitis. (medscape.com)
- Intravitreal delivery of pharmacologic agents is the key method of drug delivery for posterior segment disease including retinal vascular disorders and posterior uveitis. (medscape.com)
Differentiation1
- Studies in osteoclast biology have led to the identification of factors responsible for the differentiation and activation of osteoclasts, the most important of which is the receptor activator of NF-kappa B ligand/osteoclast differentiation factor (RANKL/ODF), a tumor necrosis factor (TNF)-like protein. (umassmed.edu)
Tumor growth2
- von Willebrand factor (vWF) is a potent regulator of angiogenesis, tumor growth, and metastasis. (biomedcentral.com)
- Research on the GC-hemostasis association has revealed that the increased expression of tissue factor (TF) promotes the pathogenic conditions of coagulation, tumor growth, and angiogenesis [ 7 ]. (biomedcentral.com)
Tumors4
- described a factor secreted by tumors causing angiogenesis and called it tumor angiogenesis factor. (wikipedia.org)
- identified a vascular permeability factor secreted by tumors in guinea pigs and hamsters. (wikipedia.org)
- Our data showed that VEGFR-3 loss-of-function is accompanied by increased vascular leakage in the retina, in solid tumors, and in the ear skin. (helsinki.fi)
- High-grade gliomas can be highly invasive and extremely vascular tumors. (ajnr.org)
Proliferation2
- Complex subunit associated factors are involved in hybridoma growth, Eosinohils, eritroid proliferation and derived from promotor binding stimulating subunits on the DNA binding complex. (cellcycl.com)
- CMMs usually progress from an in situ proliferation to a radial growth pattern, and then to a vertical growth phase. (hindawi.com)
Expression2
- Liu H, Chen Y, Yan F, Han X, Wu J, Liu X, Zheng H. Ultrasound Molecular Imaging of Vascular Endothelial Growth Factor Receptor 2 Expression for Endometrial Receptivity Evaluation. (thno.org)
- Deep RNA-DNA, RNA-protein interaction studies, and phenotype rescue analyses reveal that LETR1 is a nuclear trans-acting lncRNA modulating, via key epigenetic factors, the expression of essential target genes, including KLF4 and SEMA3C , governing the growth and migratory ability of LECs. (nature.com)
Hypoxia1
- In this study, a rat model of wound ischemia was used to test the hypothesis that HBO enhances wound healing by modulating hypoxia-inducible factor-1alpha (HIF-1alpha) signaling. (nih.gov)
Molecular1
- Environmental factors that can detect specific IgE antibodies against most low-molecular- affect the initiation of occupational asthma include the intrinsic weight agents has resulted in a search for alternative or characteristics of causative agents as well as the influence of the complementary physiopathologic mechanisms leading to airway level and route of exposure at the workplace. (cdc.gov)
Prognostic1
- Thus, the identification of biologically prognostic factors in lymphomas must be investigated (Korkolopoulou et al . (vin.com)
Inflammatory2
- High-mobility group box 1 protein (HMGB1) has been reported to be a potent proangiogenic factor induced by inflammatory stress. (molvis.org)
- Following cleavage of the precursor prepro-vWF form, the mature vWF is stored in Weibel-Palade bodies until its release is stimulated by various secretagogues or pathological stimuli, including inflammatory factors. (biomedcentral.com)
Vessel growth1
- Angiogenesis was examined by intraperitoneal injection of 5-bromodeoxyuridine (BrdU) in mice to quantify new brain vessel growth. (biomedcentral.com)
Activation1
- Binding of vascular growth factors to isoform 1 leads to the activation of several signaling cascades. (drugbank.com)