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基因敲除是通过同源重组方法定位突变细胞内某特定基因 ,使之失去功能。雌激素受体基因敲除小鼠的制备为研究雌激素的心血管作用机制提供了强有力的工具。雌激素由ERα介导促进内皮细胞依赖的血管舒张和内皮型一氧化氮合成酶表达 ,而对诱导型一氧化氮合成酶 (iNOS)的产生起抑制作用 ;相反 ,ERβ促进非内皮细胞依赖的血管舒张 ,促进iNOS产生。ERα介导雌激素对血管损伤和动脉粥样硬化的抑制作用 ,但ERβ的作用仍有争论。对ERβ基因敲除小鼠的表型研究发现 ,血管平滑肌细胞的离子通道发生变化 ,动物血压升高 ,表明ERβ在调节血管功能和高血压形成中起重要作用
Gene knockout is the homologous recombination method to locate a particular gene in a mutant cell, so that it loses its function. The preparation of estrogen receptor knockout mice provides a powerful tool for studying the cardiovascular mechanism of estrogen. Estrogen is mediated by ERa to promote endothelial-dependent vasodilatation and endothelial nitric oxide synthase expression, while inhibiting the production of inducible nitric oxide synthase (iNOS). In contrast, ERβ promotes non-endothelial dependent Vasodilation, promote iNOS production. ERα mediates the inhibitory effect of estrogen on vascular injury and atherosclerosis, but the role of ERβ remains controversial. Phenotypic studies of ERβ knockout mice revealed that changes in ion channels in vascular smooth muscle cells and elevated blood pressure in animals suggest that ERβ plays an important role in the regulation of vascular function and hypertension