Estrogen-Stimulated Endothelial Repair Requires Osteopontin
Author(s) -
Lætitia Lam Shang Leen,
Cédric Filipe,
Audrey Billon,
Barbara GarmySusini,
Sandra Jalvy,
Fanny Robbesyn,
Danièle Daret,
Cécile Allières,
Susan R. Rittling,
Nikos Werner,
Georg Nickenig,
Urban Deutsch,
Cécile Duplaà,
Pascale Dufourcq,
Françoise Lenfant,
Claude Des̀granges,
JeanFrançois Arnal,
AlainPierre Gadeau
Publication year - 2008
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.108.167965
Subject(s) - osteopontin , bone marrow , endothelial stem cell , neointima , endothelium , transplantation , cancer research , microbiology and biotechnology , osteoblast , biology , immunology , pathology , medicine , restenosis , endocrinology , stent , biochemistry , in vitro
Estradiol (E(2)) is known to accelerate reendothelialization and thus prevent intimal thickening and in-stent restenosis after angioplasty. Transplantation experiments with ERalpha(-/-) mice have previously shown that E(2) acts through local and bone marrow cell compartments to enhance endothelial healing. However, the downstream mechanisms induced by E(2) to mediate endothelial repair are still poorly understood.
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