Vascular endothelial cell-derived endothelin-1 mediates vascular inflammation and neointima formation following blood flow cessation
Author(s) -
Dyah Wulan Anggrahini,
Noriaki Emoto,
Kazuhiko Nakayama,
Bambang Widyantoro,
Suko Adiarto,
Naoko Iwasa,
Hidemi aka,
Yoshiyuki Rikitake,
Yaz Y. Kisanuki,
Masashi Yanagisawa,
Ken–ichi Hirata
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/cvp026
Subject(s) - neointima , inflammation , vascular smooth muscle , vascular remodelling in the embryo , vasoprotective , endothelin 1 , endothelial stem cell , endothelium , vasoconstriction , endothelin receptor , vascular endothelial growth factor c , medicine , vascular endothelial growth factor b , immunology , receptor , biology , vascular endothelial growth factor a , vascular endothelial growth factor , restenosis , nitric oxide , in vitro , biochemistry , smooth muscle , stent , vegf receptors
Although endothelin-1 (ET-1) has been suggested to contribute to the pathogenesis of neointima formation and atherosclerosis, the individual roles of ET-1 derived from certain cell types in this disease remain unclear. In this study, we determined the role of vascular endothelial ET-1 on vascular inflammation and neointima formation using vascular endothelial ET-1-knockout [ET-1(f/f); Tie2-Cre (+)] mice.
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