Estrogen-induced SDF-1 production is mediated by estrogen receptor-α in female hearts after acute ischemia and reperfusion.
Estrogen-induced SDF-1 production is mediated by estrogen receptor-α in female hearts after acute ischemia and reperfusion.
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DOI：
10.1016/j.surg.2011.05.010
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发表时间：
2011-08
期刊：
影响因子：
3.8
通讯作者：
Wang M
中科院分区：
文献类型：
--
作者：
Huang C;Gu H;Wang Y;Wang M
急性缺血/再灌注（I/R）损伤的心肌反应存在性别差异，雌激素介导了I/R后女性心脏的心脏保护作用。越来越多的证据表明，基质细胞衍生因子-1（SDF-1）在缺血性心脏中增加并启动心脏保护作用。然而，目前尚不清楚SDF-1是否在心肌I/R的性别特异性反应和雌激素诱导的急性保护中发挥作用。因此，我们假设：1）与男性相比，女性心脏对I/R的反应会增加SDF-1的产生，这可归因于雌激素的作用; 2）雌激素受体（ER）α，而不是ERβ介导I/R后女性心脏中雌激素贡献的SDF-1表达。评估I/R损伤的心脏组织的SDF-1（ELISA）和SDF-1受体-CXCR 4（Western印迹）的心肌表达。分组如下：成年雄性、雌性、切除卵巢的雌性以及补充长期17β-雌二醇（E2）的雄性和切除卵巢的雌性大鼠心脏，以及成年雄性和雌性野生型、ERα敲除（ERαKO）和ERβKO小鼠心脏。I/R显著增加了两种性别的心肌SDF-1表达。I/R后女性心脏中SDF-1的水平高于男性。通过卵巢切除术消耗内源性雌激素减少了I/R后女性心脏SDF-1的产生。E2的补充显着恢复SDF-1的表达在卵巢切除的女性和男性相比，他们的同行。值得注意的是，ERα而不是ERβ的消融显着减少了I/R后女性SDF-1的产生。与SDF-1不同，缺血心脏中心脏CXCR 4表达不受性别、性激素和ER的影响。我们的研究首次证明了女性心脏在急性I/R后比男性表现出更高水平的SDF-1表达。女性心肌SDF-1的产生增加部分是由于雌激素通过ERα而不是ERβ的作用。
Gender differences exist in myocardial response to acute ischemia/reperfusion (I/R) injury and estrogen mediates cardioprotection in the female heart following I/R. Accumulating evidence has indicated that stromal cell-derived factor-1 (SDF-1) is increased in the ischemic heart and initiates cardioprotective effects. However, it is unknown whether SDF-1 plays a role in gender-specific response to myocardial I/R and in estrogen-induced acute protection. Therefore, we hypothesize that: 1) increased SDF-1 production will be observed in female hearts compared to males in response to I/R, which is attributable to the effect of estrogen; 2) Estrogen receptor (ER)α, not ERβ mediates estrogen-contributed SDF-1 expression in female hearts following I/R. Heart tissue subjected to I/R injury was assessed for myocardial expression of SDF-1(ELISA) and SDF-1 receptor – CXCR4 (Western blot). Groups were as follows: rat hearts from adult male, female, ovariectomized female, and male and ovariectomized female supplemented with chronic 17β-estradiol (E2), and mouse hearts from adult male and female wildtype, ERα knockout (ERαKO) and ERβKO. I/R significantly increased myocardial SDF-1 expression in both genders. Higher levels of SDF-1 existed in female hearts after I/R compared to males. Depletion of endogenous estrogen by ovariectomy reduced cardiac SDF-1 production in females following I/R. E2 supplementation significantly restored SDF-1 expression in ovariectomized female and males compared to their counterparts. Notably, ablation of ERα, not ERβ, markedly decreased SDF-1 production in females after I/R. Unlike SDF-1, cardiac CXCR4 expression was not affected by gender, sex hormone and ERs in the ischemic heart. Our study represents the first evidence of that female hearts exhibit higher levels of SDF-1 expression compared to males after acute I/R. This increased myocardial SDF-1 production in females is partly due to effect of estrogen through ERα, not ERβ.
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影响因子：
10.8
作者：
Damås, JK;Eiken, HG;Aukrust, P
通讯作者：
Aukrust, P
影响因子：
11.2
作者：
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作者：
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DOI：
10.1073/pnas.2235866100
发表时间：
2003-11-25
影响因子：
11.1
作者：
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通讯作者：
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