Adiponectin modulates the function of endothelial progenitor cells via AMPK/eNOS signaling pathway

Endothelial progenitor cells have been shown to differentiate into endothelial cells and to play a pivotal role in vascular homeostasis. Adiponectin has anti-atherogenic and anti-inflammatory properties via directly acting on vascular cells. The aim of the present study is to explore the effect of a...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2017-11, Vol.493 (1), p.64-70
Main Authors: Wang, Shuhong, Miao, Jie, Qu, Meijie, Yang, Guo-Yuan, Shen, Linhui
Format: Article
Language:English
Subjects:
Adiponectin
Adiponectin - metabolism
AMP-Activated Protein Kinases - metabolism
AMPK
Angiogenesis
Cell Differentiation
Cell Movement - physiology
Cell Proliferation - physiology
Cells, Cultured
Endothelial progenitor cell
Endothelial Progenitor Cells - cytology
Endothelial Progenitor Cells - physiology
Gene Expression Regulation, Developmental - physiology
Humans
Neovascularization, Physiologic - physiology
Nitric Oxide Synthase Type III - metabolism
Signal Transduction - physiology
Vascular disease
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Summary:Endothelial progenitor cells have been shown to differentiate into endothelial cells and to play a pivotal role in vascular homeostasis. Adiponectin has anti-atherogenic and anti-inflammatory properties via directly acting on vascular cells. The aim of the present study is to explore the effect of adiponectin on major functions involved in survival, migration, and tube formation of endothelial progenitor cells and to explore the underlying mechanism. In this study, we transferred adiponectin gene into endothelial progenitor cells via lentiviral vectors and investigated the proliferation, migration and tube formation of these transfected cells. We found that adiponectin is highly expressed in endothelial progenitor cells and promotes their proliferation, migration and tube formation. Western blot data showed that the former two processes were mediated through the AMPK/Akt/eNOS pathway, the latter via the AMPK/eNOS pathway. Use of the AMPK inhibitor (Compound C) or Akt inhibitor (MK-2206) reduced eNOS phosphorylation and attenuated adiponectin-induced endothelial progenitor cell proliferation, migration and tube formation compared to the controls (p 
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2017.09.073