Inhibition of endothelial progenitor cell glycogen synthase kinase-3β results in attenuated neointima formation and enhanced re-endothelialization after arterial injury
Author(s) -
Benjamin Hibbert,
Xiaoli Ma,
Ali Pourdjabbar,
E. Holm,
Katey J. Rayner,
Yong-Xiang Chen,
Jiangfeng Sun,
L G Filion,
Edward R. O’Brien
Publication year - 2009
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvp156
Subject(s) - neointima , progenitor cell , gsk 3 , endothelial progenitor cell , ex vivo , medicine , microbiology and biotechnology , in vivo , biology , stem cell , kinase , restenosis , stent
Endothelial progenitor cells (EPCs) are circulating pluripotent vascular cells capable of enhancing re-endothelialization and diminishing neointima formation following arterial injury. Glycogen synthase kinase (GSK)-3beta is a protein kinase that has been implicated in the regulation of progenitor cell biology. We hypothesized that EPC abundance and function could be enhanced with the use of an inhibitor of GSK-3beta (GSKi), thereby resulting in improved arterial repair.
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