在内皮和血管光滑肌细胞中的循环氧化酶-2抑制了高脂血症小鼠中的腺体发生

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Soon Yew Tang¹, James Monslow, Leslie Todd

¹Institute for Translational Medicine and Therapeutics (S.Y.T., J.M., J.L., G.A.F.) and Perelman School of Medicine, Department of Animal Biology, School of Veterinary Medicine (L.T., E.P.), University of Pennsylvania, Philadelphia.

Circulation

|February 13, 2014

概括

血管细胞中选择性COX-2丧失加速动脉样硬化,并提高血压. 将循环氧化酶-2 (COX-2) 抑制剂向巨细胞可能会减轻与NSAID相关的心血管风险.

科学领域:

心血管科学心血管科学
药理学药理学是指药理学的学科.
分子生物学分子生物学

背景情况:

针对循环氧化酶-2 (COX-2) 的非类固醇抗炎药物 (NSAIDs) 显示出心血管风险.
全球COX-2删除在小鼠中加速动脉样硬化.
在巨细胞中选择性COX-2删除延迟了动脉动脉生成.

研究的目的:

研究COX-2在血管细胞中的作用与大细胞在动脉生成中的作用.
确定COX-2减少在特定细胞类型对心血管参数的影响.

主要方法:

在Ldlr淘汰赛小鼠的血管光滑肌细胞和内皮细胞中选择性产后删除COX-2.
对前列腺素和血小板素生物合成的分析.
评估血压和动脉样硬化病变的发展.

主要成果:

血管细胞中COX-2的枯竭减少了前列腺素I2和E2的生物合成,增加了血压,并加速了动脉动脉生成.
血管细胞中COX-2的缺失导致了病变巨细胞中COX-2表达的增加和血栓糖的升高.
病变显示原蛋白,拉米宁,α-光滑肌动蛋白和纤维化增加.

结论:

在巨细胞和血管细胞中,COX-2 具有与异的作用,涉及到动脉动脉生成.
全球COX-2抑制可能掩盖在NSAID心血管风险中观察到的细胞特异性影响.
向向巨细胞输送COX-2抑制剂可以保持有效性,同时降低心血管风险.

关键词:

在此基础上,我们进行了以太基因生成.循环氧化基因酶 (cyclooxygenase) 是一种细胞内皮细胞的内皮细胞.前列腺腺中的前列腺腺腺体血管光滑肌肉的肌肉.

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