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首页> 外文期刊>Life sciences >Effect of estrogen on calcium-handling proteins, beta-adrenergic receptors, and function in rat heart.
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Effect of estrogen on calcium-handling proteins, beta-adrenergic receptors, and function in rat heart.

机译：雌激素对大鼠心脏中钙处理蛋白，β-肾上腺素受体和功能的影响。

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Regulation of cellular Ca(2+) cycling is central to myocardial contractile function. Loss of Ca(2+) regulation is associated with cardiac dysfunction and pathology. Estrogen has been shown to modify contractile function and to confer cardioprotection. Therefore, we investigated the effect of estrogen on expression of rat heart myocardial Ca(2+)-handling proteins and beta-adrenergic receptor (beta(1)-AR) and examined functional correlates. Female rats were sham-operated (SHAM) or ovariectomized. Two weeks after ovariectomy rats were injected (i.p.) daily with estradiol benozoate (OVX+EB) or sesame oil (OVX) for 2 weeks. Protein abundance was measured by immunoblotting and mRNA was quantified by real-time RT-PCR. OVX significantly decreased estrogen and progesterone levels and EB replacement returned both estrogen and progesterone to physiological levels. OVX induced a 75% reduction of uterine weight and a gain in body weight. Replacement restored weights to SHAM level. OVX increased and estrogen-replacement normalized abundance of beta(1)-AR and L-type Ca(2+) channel (Cav1.2) protein. OVX decreased sodium-Ca(2+) exchange protein (NCX) and estrogen restored protein abundance to SHAM levels. Sarcoplasmic reticular ATPase (SERCA), phospholamban (PLB), and ryanodine receptor (RyR) abundance was not altered by hormone status. Levels of mRNA encoding for beta(1)-AR, Cav1.2, and NCX were not influenced by OVX or estrogen replacement. OVX had no effect on SERCA and PLB mRNA level but estrogen replacement elicited a significant increase compared to OVX and SHAM. Estrogen-dependent changes in Ca(2+)-handling proteins and beta(1)-AR are theoretically consistent reduced myocellular Ca(2+) load. However, hormone-dependent alterations in protein were not associated with changes in contractile function.
机译：细胞Ca（2+）循环的调节是心肌收缩功能的核心。 Ca（2+）调节的损失与心脏功能障碍和病理学相关。雌激素已被证明可以改变收缩功能并赋予心脏保护作用。因此，我们调查了雌激素对大鼠心脏心肌Ca（2+）处理蛋白和β-肾上腺素受体（beta（1）-AR）表达的影响，并检查了功能相关性。雌性大鼠假手术（SHAM）或去卵巢。卵巢切除术后两周，每天给大鼠（腹膜内）注射苯磺酸雌二醇（OVX + EB）或芝麻油（OVX）2周。通过免疫印迹测量蛋白质丰度，并通过实时RT-PCR定量mRNA。 OVX显着降低了雌激素和孕激素的水平，而EB替代使雌激素和孕激素均恢复到生理水平。 OVX引起子宫重量减少75％，体重增加。更换后的砝码恢复到SHAM水平。 OVX增加和雌激素替代标准化的beta（1）-AR和L型Ca（2+）通道（Cav1.2）蛋白的丰度。 OVX减少钠Ca（2+）交换蛋白（NCX）和雌激素恢复蛋白丰度到SHAM水平。肌浆网状ATPase（SERCA），phospholamban（PLB）和ryanodine受体（RyR）的丰度不会因激素状态而改变。编码beta（1）-AR，Cav1.2和NCX的mRNA的水平不受OVX或雌激素替代的影响。 OVX对SERCA和PLB mRNA水平无影响，但与OVX和SHAM相比，雌激素替代引起明显增加。 Ca（2+）处理蛋白和beta（1）-AR的雌激素依赖性变化是理论上一致的减少肌细胞Ca（2+）负荷。但是，激素依赖性蛋白质的改变与收缩功能的改变无关。

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