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====Overview==== {|class="wikitable" |- ! Stimulator !! Mechanism |- | [[fibroblast growth factor|FGF]] || Promotes proliferation & differentiation of endothelial cells, smooth muscle cells, and fibroblasts |- | [[vascular endothelial growth factor|VEGF]] || Affects permeability |- | [[VEGFR]] and [[NRP-1]] || Integrate survival signals |- | [[Ang1]] and [[Ang2]] || Stabilize vessels |- | [[platelet derived growth factor|PDGF]] (BB-homodimer) and [[PDGFR]] || recruit [[smooth muscle cell]]s |- | [[transforming growth factor beta|TGF-β]], [[endoglin]] and [[transforming growth factor beta receptor|TGF-β receptor]]s || ↑[[extracellular matrix]] production |- | [[CCL2]] ||Recruits [[lymphocyte]]s to sites of [[inflammation]] |- | [[Histamine]] || |- | Integrins [[alpha-v beta-3|α<sub>V</sub>β<sub>3</sub>]], [[alpha-v beta-5|α<sub>V</sub>β<sub>5</sub>]] (?<ref>Perhaps an inhibitor of angiogenesis: {{cite journal | vauthors = Sheppard D | title = Endothelial integrins and angiogenesis: not so simple anymore | journal = The Journal of Clinical Investigation | volume = 110 | issue = 7 | pages = 913–914 | date = October 2002 | pmid = 12370267 | pmc = 151161 | doi = 10.1172/JCI16713 }}</ref>) and [[alpha-5 beta-1|α<sub>5</sub>β<sub>1</sub>]] || Bind [[matrix macromolecules]] and [[proteinase]]s |- | [[VE-cadherin]] and [[CD31]] || endothelial [[junctional molecule]]s |- | [[ephrin]] || Determine formation of arteries or veins |- | [[plasminogen activator]]s || remodels [[extracellular matrix]], releases and activates growth factors |- | [[plasminogen activator inhibitor-1]] || stabilizes nearby vessels |- | [[nitric oxide synthase|eNOS]] and [[COX-2]] || |- | [[AC133]] || regulates [[angioblast]] differentiation |- | [[ID1]]/[[ID3 (gene)|ID3]] || Regulates endothelial [[transdifferentiation]] |- |Class 3 [[semaphorin]]s |Modulates endothelial cell adhesion, migration, proliferation and apoptosis. Alters vascular permeability<ref name="Mecollari_2014">{{cite journal | vauthors = Mecollari V, Nieuwenhuis B, Verhaagen J | title = A perspective on the role of class III semaphorin signaling in central nervous system trauma | journal = Frontiers in Cellular Neuroscience | volume = 8 | pages = 328 | date = 2014 | pmid = 25386118 | pmc = 4209881 | doi = 10.3389/fncel.2014.00328 | doi-access = free }}</ref> |- |Nogo-A ||Regulates endothelial cell migration and proliferation.<ref>{{cite journal | vauthors = Rust R, Grönnert L, Gantner C, Enzler A, Mulders G, Weber RZ, Siewert A, Limasale YD, Meinhardt A, Maurer MA, Sartori AM, Hofer AS, Werner C, Schwab ME | display-authors = 6 | title = Nogo-A targeted therapy promotes vascular repair and functional recovery following stroke | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 116 | issue = 28 | pages = 14270–14279 | date = July 2019 | pmid = 31235580 | pmc = 6628809 | doi = 10.1073/pnas.1905309116 | doi-access = free | bibcode = 2019PNAS..11614270R }}</ref> Alters vascular permeability.<ref>{{cite journal | vauthors = Rust R, Weber RZ, Grönnert L, Mulders G, Maurer MA, Hofer AS, Sartori AM, Schwab ME | display-authors = 6 | title = Anti-Nogo-A antibodies prevent vascular leakage and act as pro-angiogenic factors following stroke | journal = Scientific Reports | volume = 9 | issue = 1 | pages = 20040 | date = December 2019 | pmid = 31882970 | pmc = 6934709 | doi = 10.1038/s41598-019-56634-1 | bibcode = 2019NatSR...920040R | doi-access = free }}</ref> |}
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