Estradiol Enhances Recovery After Myocardial Infarction by Augmenting Incorporation of Bone Marrow–Derived Endothelial Progenitor Cells Into Sites of Ischemia-Induced Neovascularization via Endothelial Nitric Oxide Synthase–Mediated Activation of Matrix Metalloproteinase-9
Author(s) -
Atsushi Iwakura,
Shubha Shastry,
Corinne Luedemann,
Hiromichi Hamada,
Atsuhiko Kawamoto,
Raj Kishore,
Yan Zhu,
Gangjian Qin,
Marcy Silver,
Tina Thorne,
Liz Eaton,
Haruchika Masuda,
Takayuki Asahara,
Douglas W. Losordo
Publication year - 2006
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.105.553925
Subject(s) - enos , medicine , neovascularization , endocrinology , progenitor cell , ischemia , nitric oxide , bone marrow , endothelial progenitor cell , nitric oxide synthase , angiogenesis , stem cell , biology , microbiology and biotechnology
Recent data have indicated that estradiol can modulate the kinetics of endothelial progenitor cells (EPCs) via endothelial nitric oxide synthase (eNOS)-dependent mechanisms. We hypothesized that estradiol could augment the incorporation of bone marrow (BM)-derived EPCs into sites of ischemia-induced neovascularization, resulting in protection from ischemic injury.
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