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Furthermore, Greemberg et al. [ 35], demonstrated that VEGF abolished pericyte coverage of vascular sprouts, leading to vessel destabilization.
However, angiogenesis not only depends on endothelial cell invasion and proliferation, but also requires coverage of vascular sprouts by peri-endothelial cells for vessel stabilization.
Signaling initiated by VEGFR and PDGFR is fundamental for the angiogenic response [ 1, 5, 6], which comprises proliferation and invasion of endothelial cells and also formation of pericyte coverage of vascular sprouts for stabilization of the newly formed vessel walls.
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The decrease in PDGFRA expression, together with decreased vascular coverage of desmin staining, point towards reduction of the B-type pericyte [ 25] characterized by expression of these markers.> -wrap-foot> RNA isolated from vascular fragments was analyzed by real-time RT-PCR.
Increased pericyte coverage may also be an indicator of vascular dysfunction.
Coverage of vasculature by pericytes stabilizes vascular structure [ 24].
Therefore, the vascular defects and hemorrhage precede pericyte coverage of the affected vessels, suggesting that these vascular defects originate in the endothelium.
Absence of Shb promotes B16F10 tumor metastasis due to increased vascular permeability and reduced pericyte/myofibrillar cell coverage of endothelial cells, thus allowing intravasation and vascular dissemination of tumor cells.
Treatment of vascular dementia has also received extensive coverage (Broich 2003; Malouf and Birks 2004; Pantoni 2004; Schindler 2005).
Instead, there was reported increased secretion of vascular endothelial growth factor (VEGF), diminished pericyte coverage of vessels, and increased vessel leakiness and vasculogenesis.
Reduction in pericyte coverage of blood vessels leads to brain vascular defects and micro-hemorrhages (Hellström et al., 2001).
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