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Contrasting Roles of E2F2 and E2F3 in Cardiac Neovascularization

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单位: [1]Northwestern Univ, Feinberg Cardiovasc Res Inst, Dept Med Cardiol, Feinberg Sch Med, Chicago, IL 60611 USA [2]Huazhong Univ Sci & Technol, Tongji Hosp, Dept Plast Surg, Wuhan 430074, Hubei, Peoples R China [3]Huazhong Univ Sci & Technol, Tongji Med Coll, Dept Cardiol, Union Hosp, Wuhan 430074, Hubei, Peoples R China [4]Renmin Hosp, Dept Cardiol, Songzi, Hubei, Peoples R China [5]Renmin Hosp, Songzi, Hubei, Peoples R China [6]Chinese Acad Med Sci, Dept Cardiol, Cardiovasc Inst, Beijing 100730, Peoples R China [7]Chinese Acad Med Sci, Fuwai Hosp, Beijing 100730, Peoples R China [8]Peking Union Med Coll, Beijing 100021, Peoples R China
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Insufficient neovascularization, characterized by poor endothelial cell (EC) growth, contributes to the pathogenesis of ischemic heart disease and limits cardiac tissue preservation and regeneration. The E2F family of transcription factors are critical regulators of the genes responsible for cell-cycle progression and growth; however, the specific roles of individual E2Fs in ECs are not well understood. Here we investigated the roles of E2F2 and E2F3 in EC growth, angiogenesis, and their functional impact on myocardial infarction (MI). An endothelial-specific E2F3-deficient mouse strain VE-Cre; E2F3(fl/fl) was generated, and MI was surgically induced in VE-Cre; E2F3(fl/fl) and E2F2-null (E2F2 KO) mice and their wild-type (WT) littermates, VE-Cre; E2F3(+/+) and E2F2 WT, respectively. The cardiac function, infarct size, and vascular density were significantly better in E2F2 KO mice and significantly worse in VE-Cre; E2F3(fl/fl) mice than in their WT littermates. The loss of E2F2 expression was associated with an increase in the proliferation of ECs both in vivo and in vitro, while the loss of E2F3 expression led to declines in EC proliferation. Thus, E2F3 promotes while E2F2 suppresses ischemic cardiac repair through corresponding changes in EC proliferation; and differential targeting of specific E2F members may provide a novel strategy for therapeutic angiogenesis of ischemic heart disease.

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出版当年[2012]版:
大类 | 2 区 生物
小类 | 2 区 生物学
最新[2025]版:
大类 | 3 区 综合性期刊
小类 | 3 区 综合性期刊
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出版当年[2011]版:
Q1 BIOLOGY
最新[2023]版:
Q1 MULTIDISCIPLINARY SCIENCES

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第一作者单位: [1]Northwestern Univ, Feinberg Cardiovasc Res Inst, Dept Med Cardiol, Feinberg Sch Med, Chicago, IL 60611 USA
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