The role of pericytes in angiogenesis

Ribatti, Doménico; Crivellato, Enrico

doi:10.1387/ijdb.103167dr

Cited by 372 publications

(270 citation statements)

References 82 publications

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“…The vessel is supported by pericytes which 6 use web-like extremities to envelope the vessel [19] and an outer layer of vascular smooth muscle (VSM) and adventitial fibroblasts [20]. The maintenance of vessel growth and expansion within the bronchial vasculature are regulated by an array of cell types ranging from endothelial progenitor cells (EPCs), to the mural cells which support the vessels, and airway structural cells such as ASM cells and fibroblasts, as summarised in figure 2.…”

Section: Cellular Composition Of the Pulmonary Vasculature Systemmentioning

confidence: 99%

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Pulmonary vascular changes in asthma and COPD

Harkness

Kanabar

Sharma

et al. 2014

Pulmonary Pharmacology & Therapeutics

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In chronic lung disorders such as in asthma and chronic obstructive pulmonary disease (COPD) there is increased bronchial angiogenesis and remodelling of pulmonary vessels culminating to altered bronchial and pulmonary circulation. The involvement of residential cells such as endothelial cells, smooth muscle cells and pulmonary fibroblasts, all appear to have a crucial role in the progression of vascular inflammation and remodelling. The regulatory abnormalities, growth factors and mediators implicated in the pulmonary vascular changes of asthma and COPD subjects and potential therapeutic targets have been described in this review.

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Section: Cellular Composition Of the Pulmonary Vasculature Systemmentioning

confidence: 99%

“…Pericytes not only provide a vital structural support, these cells are central to the process of angiogenesis [19]. Upon activation by inflammation, hypoxia or shear stress [32], pericytes then activate endothelial cells to proliferate with the release of mediators [30,31], and commence the angiogenic process.…”

Section: Pericytes and Vascular Smooth Muscle Cellsmentioning

confidence: 99%

Pulmonary vascular changes in asthma and COPD

Harkness

Kanabar

Sharma

et al. 2014

Pulmonary Pharmacology & Therapeutics

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“…MCs include pericytes and smooth muscle cells (SMCs), although a clear distinction between these 2 cell types remains controversial. 2 Mechanisms involved in their recruitment on endothelial sprouts are complex. Pericytes are proposed to originate from surrounding mesenchymal precursors or to be recruited from the wall of adjacent vessels before differentiating into SMCs.…”

Section: Introductionmentioning

confidence: 99%

Sonic hedgehog mediates a novel pathway of PDGF-BB–dependent vessel maturation

Yao

Renault

Chapouly

et al. 2014

Blood

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“…Endothelial cells of arteries and veins are surrounded by VSMCs, whereas those of capillaries are surrounded by pericytes (12). Completion of angiogenesis requires envelopment of new vessels by pericytes or VSMCs, which express α-smooth muscle actin (αSMA) and tropomyosin (11)(12)(13).…”

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confidence: 99%

Long-acting progestin-only contraceptives impair endometrial vasculature by inhibiting uterine vascular smooth muscle cell survival

Kayisli

Başar

Guzeloglu‐Kayisli

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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Molecular mechanisms responsible for abnormal endometrial vasculature in women receiving long-acting progestin-only contraceptives (LAPCs) are unknown. We hypothesize that LAPCs impair vascular smooth muscle cell (VSMC) and pericyte proliferation and migration producing thin-walled hyperdilated fragile microvessels prone to bleeding. Proliferating cell nuclear antigen (PCNA) and α-smooth muscle actin (αSMA) double-immunostaining assessed VSMC differentiation and proliferation in endometria from women before and after DepoProvera (Depo) treatment and from oophorectomized guinea pigs (OVX-GPs) treated with vehicle, estradiol (E2), medroxyprogesterone acetate (MPA), or E2+MPA. Wholegenome profiling, proliferation, and migration assays were performed on cultured VSMCs treated with MPA or etonogestrel (ETO). Endometrial vessels of Depo-administered women displayed reduced αSMA immunoreactivity and fewer PCNA (+) nuclei among αSMA (+) cells (P < 0.008). Microarray analysis of VSMCs identified several MPA-and ETO-altered transcripts regulated by STAT1 signaling (P < 2.22 × 10 −6 ), including chemokine (C-C motif) ligand 2 (CCL2). Both MPA and ETO reduce VSMC proliferation and migration (P < 0.001). Recombinant CCL2 reversed this progestin-mediated inhibition, whereas a STAT1 inhibitor abolished the CCL2 effect. Similarly, the endometria of MPA treated OVX-GPs displayed decreased αSMA staining and fewer PCNA (+) nuclei in VSMC (P < 0.005). In conclusion, LAPCs promote abnormal endometrial vessel formation by inhibiting VSMC proliferation and migration.progestin contraceptives | abnormal uterine bleeding | VSMC | impaired vascular maturation | proliferation

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The role of pericytes in angiogenesis

Cited by 372 publications

References 82 publications

Pulmonary vascular changes in asthma and COPD

Pulmonary vascular changes in asthma and COPD

Sonic hedgehog mediates a novel pathway of PDGF-BB–dependent vessel maturation

Long-acting progestin-only contraceptives impair endometrial vasculature by inhibiting uterine vascular smooth muscle cell survival

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