Vascular Endothelial Growth Factor D
Vascular Endothelial Growth Factor A
Vascular Endothelial Growth Factors
Complement Factor D
Endothelial Growth Factors
Vascular Endothelial Growth Factor Receptor-2
Receptors, Vascular Endothelial Growth Factor
Lymphokines
Vascular Endothelial Growth Factor Receptor-1
Rosacea
Erythema
Facial Dermatoses
Telangiectasis
Drug Eruptions
c-fos-induced growth factor/vascular endothelial growth factor D induces angiogenesis in vivo and in vitro. (1/188)
c-fos-induced growth factor/vascular endothelial growth factor D (Figf/Vegf-D) is a secreted factor of the VEGF family that binds to the vessel and lymphatic receptors VEGFR-2 and VEGFR-3. Here we report that Figf/Vegf-D is a potent angiogenic factor in rabbit cornea in vivo in a dose-dependent manner. In vitro Figf/Vegf-D induces tyrosine phosphorylation of VEGFR-2 and VEGFR-3 in primary human umbilical cord vein endothelial cells (HUVECs) and in an immortal cell line derived from Kaposi's sarcoma lesion (KS-IMM). The treatment of HUVECs with Figf/Vegf-D induces dose-dependent cell growth. Figf/VEGF-D also induces HUVEC elongation and branching to form an extensive network of capillary-like cords in three-dimensional matrix. In KS-IMM cells Figf/Vegf-D treatment results in dose-dependent mitogenic and motogenic activities. Taken together with the previous observations that Figf/Vegf-D expression is under the control of the nuclear oncogene c-fos, our data uncover a link between a nuclear oncogene and angiogenesis, suggesting that Figf/Vegf-D may play a critical role in tumor cell growth and invasion. (+info)Biosynthesis of vascular endothelial growth factor-D involves proteolytic processing which generates non-covalent homodimers. (2/188)
Vascular endothelial growth factor-D (VEGF-D) binds and activates the endothelial cell tyrosine kinase receptors VEGF receptor-2 (VEGFR-2) and VEGF receptor-3 (VEGFR-3), is mitogenic for endothelial cells, and shares structural homology and receptor specificity with VEGF-C. The primary translation product of VEGF-D has long N- and C-terminal polypeptide extensions in addition to a central VEGF homology domain (VHD). The VHD of VEGF-D is sufficient to bind and activate VEGFR-2 and VEGFR-3. Here we report that VEGF-D is proteolytically processed to release the VHD. Studies in 293EBNA cells demonstrated that VEGF-D undergoes N- and C-terminal cleavage events to produce numerous secreted polypeptides including a fully processed form of M(r) approximately 21,000 consisting only of the VHD, which is predominantly a non-covalent dimer. Biosensor analysis demonstrated that the VHD has approximately 290- and approximately 40-fold greater affinity for VEGFR-2 and VEGFR-3, respectively, compared with unprocessed VEGF-D. In situ hybridization demonstrated that embryonic lung is a major site of expression of the VEGF-D gene. Processed forms of VEGF-D were detected in embryonic lung indicating that VEGF-D is proteolytically processed in vivo. (+info)A mutant form of vascular endothelial growth factor (VEGF) that lacks VEGF receptor-2 activation retains the ability to induce vascular permeability. (3/188)
Vascular endothelial growth factor (VEGF) is a major mediator of vasculogenesis and angiogenesis both during development and in pathological conditions. VEGF has a variety of effects on vascular endothelium, including the ability to stimulate endothelial cell mitogenesis, and the potent induction of vascular permeability. These activities are at least in part mediated by binding to two high affinity receptors, VEGFR-1 and VEGFR-2. In this study we have made mutations of mouse VEGF in order to define the regions that are required for VEGFR-2-mediated functions. Development of a bioassay, which responds only to signals generated by cross-linking of VEGFR-2, has allowed evaluation of these mutants for their ability to activate VEGFR-2. One mutant (VEGF0), which had amino acids 83-89 of VEGF substituted with the analogous region of the related placenta growth factor, demonstrated significantly reduced VEGFR-2 binding compared with wild type VEGF, indicating that this region was required for VEGF-VEGFR-2 interaction. Intriguingly, when this mutant was evaluated in a Miles assay for its ability to induce vascular permeability, no difference was found when compared with wild type VEGF. In addition we have shown that the VEGF homology domain of the structurally related growth factor VEGF-D is capable of binding to and activating VEGFR-2 but has no vascular permeability activity, indicating that VEGFR-2 binding does not correlate with permeability activity for all VEGF family members. These data suggest different mechanisms for VEGF-mediated mitogenesis and vascular permeability and raise the possibility of an alternative receptor mediating vascular permeability. (+info)Monoclonal antibodies to vascular endothelial growth factor-D block its interactions with both VEGF receptor-2 and VEGF receptor-3. (4/188)
Vascular endothelial growth factor-D (VEGF-D), the most recently discovered mammalian member of the VEGF family, is an angiogenic protein that activates VEGF receptor-2 (VEGFR-2/Flk1/KDR) and VEGFR-3 (Flt4). These receptor tyrosine kinases, localized on vascular and lymphatic endothelial cells, signal for angiogenesis and lymphangiogenesis. VEGF-D consists of a central receptor-binding VEGF homology domain (VHD) and N-terminal and C-terminal propeptides that are cleaved from the VHD to generate a mature, bioactive form consisting of dimers of the VHD. Here we report characterization of mAbs raised to the VHD of human VEGF-D in order to generate VEGF-D antagonists. The mAbs bind the fully processed VHD with high affinity and also bind unprocessed VEGF-D. We demonstrate, using bioassays for the binding and cross-linking of VEGFR-2 and VEGFR-3 and biosensor analysis with immobilized receptors, that one of the mAbs, designated VD1, is able to compete potently with mature VEGF-D for binding to both VEGFR-2 and VEGFR-3 for binding to mature VEGF-D. This indicates that the binding epitopes on VEGF-D for these two receptors may be in close proximity. Furthermore, VD1 blocks the mitogenic response of human microvascular endothelial cells to VEGF-D. The anti-(VEGF-D) mAbs raised to the bioactive region of this growth factor will be powerful tools for analysis of the biological functions of VEGF-D. (+info)Expression of vascular endothelial growth factors A, B, C, and D and their relationships to lymph node status in lung adenocarcinoma. (5/188)
Vascular endothelial growth factors (VEGFs) C and D are novel members of the VEGF family that show some selectivity toward lymphatic endothelial cells. Recent studies suggest that VEGF-C may be involved in lymphangiogenesis and spread of cancer cells via lymphatic vessels. However, whether other VEGF family members play a role in lymph node metastasis is largely unknown. The aim of the present study was to explore whether expressions of VEGF-A, VEGF-B, VEGF-C, and VEGF-D are correlated with lymph node status in lung adenocarcinoma. Total RNA was isolated from 60 surgical specimens of lung adenocarcinoma with (n = 27) or without (n = 33) lymph node metastasis. The relative mRNA abundance of VEGF-A, VEGF-B, VEGF-C, and VEGF-D was measured by real-time reverse transcription-PCR analysis based on TaqMan fluorescence methodology. We found that, as single factors, expression of none of the four VEGF family members clearly correlated with the presence of lymph node metastasis. The only tendency noted was for higher VEGF-B and VEGF-C and lower VEGF-D levels in the node-positive group. However, two-way scatterplot analysis revealed that tumors with lymph node metastasis were associated with a pattern of low VEGF-D and high VEGF-A, VEGF-B, or VEGF-C, such that the ratios of VEGF-D:VEGF-A, VEGF-D:VEGF-B, or VEGF-D:VEGF-C were significantly lower in the node-positive group. Strikingly, none of the 11 tumors with high VEGF-D levels metastasized to lymph nodes. Furthermore, a low VEGF-D:VEGF-C ratio correlated with the presence of lymphatic invasion, and six of seven tumors with a pattern of very high expression of VEGF-C and low expression of VEGF-D displayed lymph vessel invasion that extended along the bronchovascular tree beyond the main tumor. Finally, levels of VEGF-A, but not VEGF-B or VEGF-C, were higher in tumors with large nodal metastasis (> or = 1 cm) than in those with small (< 1 cm) nodal metastasis. These results support the hypothesis that two VEGF family members are involved in lymph node metastasis at two distinct steps; VEGF-C facilitates entry of cancer cells into the lymph vasculature, whereas VEGF-A promotes the growth of metastatic tumor through angiogenesis. The results also suggest that the balance between VEGF-C and VEGF-D could be important rather than the level of VEGF-C alone. Whether a low VEGF-D level plays a causative role in lymph node metastasis requires further investigation. (+info)VEGF-C and VEGF-D expression in neuroendocrine cells and their receptor, VEGFR-3, in fenestrated blood vessels in human tissues. (6/188)
Recently, vascular endothelial growth factor receptor 3 (VEGFR-3) has been shown to provide a specific marker for lymphatic endothelia in certain human tissues. In this study, we have investigated the expression of VEGFR-3 and its ligands VEGF-C and VEGF-D in fetal and adult tissues. VEGFR-3 was consistently detected in the endothelium of lymphatic vessels such as the thoracic duct, but fenestrated capillaries of several organs including the bone marrow, splenic and hepatic sinusoids, kidney glomeruli and endocrine glands also expressed this receptor. VEGF-C and VEGF-D, which bind both VEGFR-2 and VEGFR-3 were expressed in vascular smooth muscle cells. In addition, intense cytoplasmic staining for VEGF-C was observed in neuroendocrine cells such as the alpha cells of the islets of Langerhans, prolactin secreting cells of the anterior pituitary, adrenal medullary cells, and dispersed neuroendocrine cells of the gastrointestinal tract. VEGF-D was observed in the innermost zone of the adrenal cortex and in certain dispersed neuroendocrine cells. These results suggest that VEGF-C and VEGF-D have a paracrine function and perhaps a role in peptide release from secretory granules of certain neuroendocrine cells to surrounding capillaries. (+info)In fibroblasts Vegf-D expression is induced by cell-cell contact mediated by cadherin-11. (7/188)
Vascular endothelial growth factors (VEGFs) are a highly conserved family of growth factors all angiogenic in vivo with mitogenic and chemotactic activity on endothelial cells. VEGFs are expressed in fibroblasts either in hypoxia or in response to growth factors. Here we report that, differently from the other members of the family, Vegf-D is induced by cell-cell contact. By in situ hybridization we demonstrated that noninteracting fibroblasts express low levels of Vegf-D mRNA, whereas contacting cells express high levels of Vegf-D transcripts. By immunostaining we observed that the surface protein cadherin-11 is localized at the opposite sites of interacting cell surfaces. Ca(2+) deprivation from the culture medium determined the loss of cadherin-11 from the cell surfaces and down-regulation of Vegf-D mRNA. Moreover, a cadherin-11 antisense RNA construct inhibited Vegf-D expression in confluent BALB/c fibroblasts, whereas in NIH 3T3 cells, which express low levels of cadherin-11, Vegf-D induction could be obtained by overexpression of cadherin-11. This suggests that cell interaction mediated by cadherin-11 induces the expression of the angiogenic factor Vegf-D in fibroblasts. (+info)Signalling via vascular endothelial growth factor receptor-3 is sufficient for lymphangiogenesis in transgenic mice. (8/188)
Vascular endothelial growth factor receptor-3 (VEGFR-3) has an essential role in the development of embryonic blood vessels; however, after midgestation its expression becomes restricted mainly to the developing lymphatic vessels. The VEGFR-3 ligand VEGF-C stimulates lymphangiogenesis in transgenic mice and in chick chorioallantoic membrane. As VEGF-C also binds VEGFR-2, which is expressed in lymphatic endothelia, it is not clear which receptors are responsible for the lymphangiogenic effects of VEGF-C. VEGF-D, which binds to the same receptors, has been reported to induce angiogenesis, but its lymphangiogenic potential is not known. In order to define the lymphangiogenic signalling pathway we have created transgenic mice overexpressing a VEGFR-3-specific mutant of VEGF-C (VEGF-C156S) or VEGF-D in epidermal keratinocytes under the keratin 14 promoter. Both transgenes induced the growth of lymphatic vessels in the skin, whereas the blood vessel architecture was not affected. Evidence was also obtained that these growth factors act in a paracrine manner in vivo. These results demonstrate that stimulation of the VEGFR-3 signal transduction pathway is sufficient to induce specifically lymphangiogenesis in vivo. (+info)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.
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.
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.
Complement Factor D is a protein that plays a crucial role in the complement system, which is a part of the immune system that helps to clear pathogens and damaged cells from the body. Specifically, Factor D is a serine protease that is involved in the alternative pathway of the complement system.
In this pathway, Factor D helps to cleave another protein called Factor B, which then activates a complex called the C3 convertase. The C3 convertase cleaves complement component 3 (C3) into C3a and C3b, leading to the formation of the membrane attack complex (MAC), which creates a pore in the membrane of the target cell, causing its lysis and removal from the body.
Deficiencies or mutations in Complement Factor D can lead to an impaired alternative pathway and increased susceptibility to certain infections, particularly those caused by Neisseria bacteria. Additionally, abnormal regulation of the complement system has been implicated in a variety of diseases, including autoimmune disorders, inflammatory conditions, and neurodegenerative diseases.
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 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.
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 - Wikipedia
VEGFD vascular endothelial growth factor D [Homo sapiens (human)] - Gene - NCBI
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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)