These analyses showed that Angiopoietin - 2 is not just affecting angiogenesis, but controls at the same time the production of tumor promoting growth
factors in endothelial cells.
The scientists in Augustin's laboratory consequently pursued preclinical tumor therapy experiments, which were aimed at not just blocking angiogenesis, but to also suppress the production of tumor - promoting growth
factors in endothelial cells.
Not exact matches
A critical discovery
in this research was finding that the novel progenitor has a receptor protein on its
cell surface called KDR, or vascular
endothelial growth
factor receptor 2, which until now, was thought to be restricted to
endothelial cells that form vessels, the progenitors for
endothelial cells and the progenitors blood
cells.
«ECPR and a
factor in the blood called protein C act as a «brake» on blood coagulation and
endothelial cell inflammation and also enhance the viability and integrity of blood vessels, but when the malaria parasites use PfEMP1 to bind EPCR, they may interfere with the normal function of EPCR, and thus the binding can be the catalyst for the violent reaction,» he explains.
The classical concepts of angiogenesis consider the
endothelial cells within tumors as a rather passive
cell population that merely reacts
in response to growth
factors released by the tumor
cells.
Due to the lack of oxygen
in the cancer
cells, VEGF - A (Vascular
Endothelial Growth
Factor) is formed and this promotes the formation of new blood vessels to supply the tumor.
In addition, when these transcription
factors lose their function, terminal differentiation into the vascular endothelium (completion of differentiation) is completely suppressed, and genes that are key to differentiation into vascular
endothelial cells as well as transcription
factors that maintain the undifferentiated state are adversely induced.
High Serum Vascular
Endothelial Growth
Factor (VEGF) Level Is An Adverse Prognostic
Factor In High Risk Diffuse Large B -
Cell Lymphoma (DLBCL) Patients Treated with Dose - Dense Chemoimmunotherapy and Systemic CNS Prophylaxis.
The resulting
endothelial cell lines described
in this study retain their phenotype after repeated passage, require minimal nutritional support and, importantly, may be useful for identifying
factors that regulate
endothelial cell proliferation and tumor
cell adhesion
in different anatomical regions.
The immortalized
endothelial cell lines established from H - 2Kb - tsA58 mice provide, for the first time, a
cell culture system to examine
factors regulating angiogenesis and tumor
cell arrest
in different organ systems.
Angiopoietin - 2 functions as an autocrine protective
factor in stressed
endothelial cells.
Expression of angiopoietin - 1
in hypoxic pericytes: regulation by hypoxia - inducible
factor - 2alpha and participation
in endothelial cell migration and tube formation.
Production of
factor VIII by human liver sinusoidal
endothelial cells transplanted
in immunodeficient uPA mice.
Other research has shown that oxygen - deprived
cells in the retina produce a type of protein called vascular
endothelial growth
factor (VEGF), which triggers the growth of new blood vessels
in the retina.
Vascular
endothelial growth
factor (VEGF) expressed by neural progenitor
cells (NPCs)(cyan) stimulates the growth of blood vessels (red)
in the mouse embryonic hindbrain, and provides regulatory
factors to promote the self - renewal of neural progenitors.
The researchers found that, when stimulated by insulin, diabetic fibroblasts produced less of the VEGF (vascular
endothelial growth
factor) signaling protein, a key player
in boosting the growth of blood vessel
cells, than normal fibroblasts did.
Susan Amara, USA - «Regulation of transporter function and trafficking by amphetamines, Structure - function relationships
in excitatory amino acid transporters (EAATs), Modulation of dopamine transporters (DAT) by GPCRs, Genetics and functional analyses of human trace amine receptors» Tom I. Bonner, USA (Past Core Member)- Genomics, G protein coupled receptors Michel Bouvier, Canada - Molecular Pharmacology of G protein - Coupled Receptors; Molecular mechanisms controlling the selectivity and efficacy of GPCR signalling Thomas Burris, USA - Nuclear Receptor Pharmacology and Drug Discovery William A. Catterall, USA (Past Core Member)- The Molecular Basis of Electrical Excitability Steven Charlton, UK - Molecular Pharmacology and Drug Discovery Moses Chao, USA - Mechanisms of Neurotophin Receptor Signaling Mark Coles, UK - Cellular differentiation, human embryonic stem
cells, stromal
cells, haematopoietic stem
cells, organogenesis, lymphoid microenvironments, develomental immunology Steven L. Colletti, USA Graham L Collingridge, UK Philippe Delerive, France - Metabolic Research (diabetes, obesity, non-alcoholic fatty liver, cardio - vascular diseases, nuclear hormone receptor, GPCRs, kinases) Sir Colin T. Dollery, UK (Founder and Past Core Member) Richard M. Eglen, UK Stephen M. Foord, UK David Gloriam, Denmark - GPCRs, databases, computational drug design, orphan recetpors Gillian Gray, UK Debbie Hay, New Zealand - G protein - coupled receptors, peptide receptors, CGRP, Amylin, Adrenomedullin, Migraine, Diabetes / obesity Allyn C. Howlett, USA Franz Hofmann, Germany - Voltage dependent calcium channels and the positive inotropic effect of beta adrenergic stimulation; cardiovascular function of cGMP protein kinase Yu Huang, Hong Kong -
Endothelial and Metabolic Dysfunction, and Novel Biomarkers
in Diabetes, Hypertension, Dyslipidemia and Estrogen Deficiency, Endothelium - derived Contracting
Factors in the Regulation of Vascular Tone, Adipose Tissue Regulation of Vascular Function
in Obesity, Diabetes and Hypertension, Pharmacological Characterization of New Anti-diabetic and Anti-hypertensive Drugs, Hypotensive and antioxidant Actions of Biologically Active Components of Traditional Chinese Herbs and Natural Plants including Polypehnols and Ginsenosides Adriaan P. IJzerman, The Netherlands - G protein - coupled receptors; allosteric modulation; binding kinetics Michael F Jarvis, USA - Purines and Purinergic Receptors and Voltage-gated ion channel (sodium and calcium) pharmacology Pain mechanisms Research Reproducibility Bong - Kiun Kaang, Korea - G protein - coupled receptors; Glutamate receptors; Neuropsychiatric disorders Eamonn Kelly, Prof, UK - Molecular Pharmacology of G protein - coupled receptors,
in particular opioid receptors, regulation of GPCRs by kinasis and arrestins Terry Kenakin, USA - Drug receptor pharmacodynamics, receptor theory Janos Kiss, Hungary - Neurodegenerative disorders, Alzheimer's disease Stefan Knapp, Germany - Rational design of highly selective inhibitors (so call chemical probes) targeting protein kinases as well as protein interaction inhibitors of the bromodomain family Andrew Knight, UK Chris Langmead, Australia - Drug discovery, GPCRs, neuroscience and analytical pharmacology Vincent Laudet, France (Past Core Member)- Evolution of the Nuclear Receptor / Ligand couple Margaret R. MacLean, UK - Serotonin, endothelin, estrogen, microRNAs and pulmonary hyperten Neil Marrion, UK - Calcium - activated potassium channels, neuronal excitability Fiona Marshall, UK - GPCR molecular pharmacology, structure and drug discovery Alistair Mathie, UK - Ion channel structure, function and regulation, pain and the nervous system Ian McGrath, UK - Adrenoceptors; autonomic transmission; vascular pharmacology Graeme Milligan, UK - Structure, function and regulation of G protein - coupled receptors Richard Neubig, USA (Past Core Member)- G protein signaling; academic drug discovery Stefan Offermanns, Germany - G protein - coupled receptors, vascular / metabolic signaling Richard Olsen, USA - Structure and function of GABA - A receptors; mode of action of GABAergic drugs including general anesthetics and ethanol Jean - Philippe Pin, France (Past Core Member)- GPCR - mGLuR - GABAB - structure function relationship - pharmacology - biophysics Helgi Schiöth, Sweden David Searls, USA - Bioinformatics Graeme Semple, USA - GPCR Medicinal Chemistry Patrick M. Sexton, Australia - G protein - coupled receptors Roland Staal, USA - Microglia and neuroinflammation
in neuropathic pain and neurological disorders Bart Staels, France - Nuclear receptor signaling
in metabolic and cardiovascular diseases Katerina Tiligada, Greece - Immunopharmacology, histamine, histamine receptors, hypersensitivity, drug allergy, inflammation Georg Terstappen, Germany - Drug discovery for neurodegenerative diseases with a focus on AD Mary Vore, USA - Activity and regulation of expression and function of the ATP - binding cassette (ABC) transporters
Three recent experimental studies focused on low consumption / exposure.949596
In one study, 29 smokers each consumed a single cigarette, immediately after which they had a significant decrease in blood vessel output power and significant increase in blood vessel ageing level and remaining blood volume 25 minutes later, as markers of atherosclerosis.94 In another study, human coronary artery endothelial cells were exposed to the smoke equivalent to one cigarette, which led to activation of oxidant stress sensing transcription factor NFR2 and up - regulation of cytochrome p450, considered to have a role in the development of heart disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.
In one study, 29 smokers each consumed a single cigarette, immediately after which they had a significant decrease
in blood vessel output power and significant increase in blood vessel ageing level and remaining blood volume 25 minutes later, as markers of atherosclerosis.94 In another study, human coronary artery endothelial cells were exposed to the smoke equivalent to one cigarette, which led to activation of oxidant stress sensing transcription factor NFR2 and up - regulation of cytochrome p450, considered to have a role in the development of heart disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.
in blood vessel output power and significant increase
in blood vessel ageing level and remaining blood volume 25 minutes later, as markers of atherosclerosis.94 In another study, human coronary artery endothelial cells were exposed to the smoke equivalent to one cigarette, which led to activation of oxidant stress sensing transcription factor NFR2 and up - regulation of cytochrome p450, considered to have a role in the development of heart disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.
in blood vessel ageing level and remaining blood volume 25 minutes later, as markers of atherosclerosis.94
In another study, human coronary artery endothelial cells were exposed to the smoke equivalent to one cigarette, which led to activation of oxidant stress sensing transcription factor NFR2 and up - regulation of cytochrome p450, considered to have a role in the development of heart disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.
In another study, human coronary artery
endothelial cells were exposed to the smoke equivalent to one cigarette, which led to activation of oxidant stress sensing transcription
factor NFR2 and up - regulation of cytochrome p450, considered to have a role
in the development of heart disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.
in the development of heart disease.95 These effects were not seen when heart
cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain
cells.96
This activates the mast
cells in these organs so that they undergo degranulation, releasing ready - made proteases such as chymase and tryptase, and synthesizing inflammatory mediators (leukotrienes and vascular
endothelial cell growth
factor [VEGF]-RRB-.
At the same time, the protein Vascular
Endothelial Growth
Factor (VEGF) stimulates blood supply for the damaged tissue, Fibroblast Growth
Factor - 2 (FGF - 2) stimulates the damaged
cells to grow and reproduce themselves, Transforming Growth
Factor - beta (TGF - beta) stimulates cartilage to grow, and Stem
Cell Factor (SCF) stimulates your native inactive stem
cells to become activated and assist
in the repair of the damaged tissue.
Researchers report that curcumin reduces all pro-inflammatory molecules
in cartilage
cells and
in membranes that line the joints, among them tumor necrosis
factor — which destroys joint cartilage — and vascular
endothelial growth
factor, which promotes excessive growth of blood vessels
in inflamed joints.
Evaluation of von Willebrand
factor as a marker of
endothelial cell reactivity
in cats with sepsis or systemic inflammatory response syndrome.