Impaired left-ventricular cardiac function in male GPR30-deficient mice
Impaired left-ventricular cardiac function in male GPR30-deficient mice
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DOI：
10.3892/mmr.2010.402
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发表时间：
2011-01-01
影响因子：
3.4
通讯作者：
Otto, Christane
中科院分区：
文献类型：
--
作者：
Delbeck, Martina;Golz, Stefan;Otto, Christane
G蛋白偶联受体30（GPR30）已被报道作为一种膜结合的雌激素受体，参与非基因组雌二醇信号转导的介导。在这项研究中，我们证明了雄性，而不是雌性，GPR30缺陷小鼠患有左心室心脏功能受损。雄性突变小鼠的左心室增大。心脏瓣膜或流出道无畸形。GPR30缺陷小鼠的左心室收缩和舒张能力均降低，导致左心室舒张末期压升高。总之，我们的数据支持GPR30在心力衰竭的性别特异性方面的作用。
G-protein-coupled receptor 30 (GPR30) has been reported to act as a membrane-bound estrogen receptor that is involved in the mediation of non-genomic estradiol signalling. In this study, we demonstrated that male, but not female, GPR30-deficient mice suffer from impaired left-ventricular cardiac function. Left ventricles from male mutant mice were enlarged. There were no malformations in the valves or outflow tract of the heart. Both the contractility and relaxation capacity of the left ventricle were reduced, leading to increased left-ventricular end-diastolic pressure in GPR30-deficient mice. In conclusion, our data support a role for GPR30 in the gender-specific aspects of heart failure.