Extracellular Vesicles Activate a CD36-Dependent Signaling Pathway to Inhibit Microvascular Endothelial Cell Migration and Tube Formation | Zendy

Devi Prasadh Ramakrishnan | Zendy; Rula A. HajjAli | Zendy; Yiliang Chen | Zendy; Roy L. Silverstein | Zendy

Open Access

Extracellular Vesicles Activate a CD36-Dependent Signaling Pathway to Inhibit Microvascular Endothelial Cell Migration and Tube Formation

Author(s) -

Devi Prasadh Ramakrishnan,

Rula A. HajjAli,

Yiliang Chen,

Roy L. Silverstein

Publication year - 2016

Publication title -

arteriosclerosis thrombosis and vascular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.007

H-Index - 270

eISSN - 1524-4636

pISSN - 1079-5642

DOI - 10.1161/atvbaha.115.307085

Subject(s) - cd36 , endothelial stem cell , matrigel , microbiology and biotechnology , umbilical vein , human umbilical vein endothelial cell , phosphatidylserine , annexin , angiogenesis , biology , chemistry , cell , biochemistry , in vitro , receptor , cancer research , phospholipid , membrane

Literature on the effect of cell-derived extracellular vesicles (EV), ≤1 μm vesicles shed from various cell types during activation or apoptosis, on microvascular endothelial cell (MVEC) signaling is conflicting. Thrombospondin-1 and related proteins induce anti-angiogenic signals in MVEC via CD36. CD36 binds EV via phosphatidylserine exposed on their surface but the effects of this interaction on MVEC functions are not known. We hypothesized that EV would inhibit angiogenic MVEC functions via CD36.

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