血管紧张素 II 通过增强 ROS 产生上调大鼠心肌细胞 cyclophilin A。
Angiotensin II upregulates cyclophilin A by enhancing ROS production in rat cardiomyocytes.
机构信息
Key Laboratory for Animal Genetic Diversity and Evolution of High Education in Yunnan Province, School of Life Sciences, Yunnan University, Kunming, Yunnan 650091, P.R. China.
Department of Emergency Medicine, The Second Affiliated Hospital, Kunming Medical University, Kunming, Yunnan 650101, P.R. China.
出版信息
Mol Med Rep. 2018 Nov;18(5):4349-4355. doi: 10.3892/mmr.2018.9448. Epub 2018 Sep 4.
Angiotensin II (Ang II) is a principal molecule of the renin‑angiotensin system, which promotes hypertrophy and fibrosis. It has been demonstrated that Ang II upregulates the expression of cyclophilin A (CypA), which is a potential myocardial hypertrophy factor. However, the mechanisms by which Ang II induces the expression of CypA in cardiomyocytes remain unclear. In the present study, reactive oxygen species (ROS) were detected by fluorescence microscopy, and western blot analysis and ELISA were used to measure CypA expression. It was identified that Ang II enhanced the production of ROS in rat cardiomyocytes. ROS, in turn, promoted CypA expression and secretion. Notably, the action of Ang II was primarily dependent on the angiotensin type 2 receptor (AT2R), not the type 1 receptor. These results provided an insight into the role of the AT2R signaling pathway in Ang II‑induced myocardial hypertrophy.
血管紧张素 II（Ang II）是肾素-血管紧张素系统的主要分子，可促进肥大和纤维化。已经证明，Ang II 上调亲环素 A（CypA）的表达，CypA 是潜在的心肌肥大因子。然而，Ang II 诱导心肌细胞中 CypA 表达的机制尚不清楚。在本研究中，通过荧光显微镜检测活性氧（ROS），并通过 Western blot 分析和 ELISA 测量 CypA 的表达。结果表明，Ang II 增强了大鼠心肌细胞中 ROS 的产生。ROS 反过来又促进了 CypA 的表达和分泌。值得注意的是，Ang II 的作用主要依赖于血管紧张素 II 型受体（AT2R），而不是 1 型受体。这些结果为 AT2R 信号通路在 Ang II 诱导的心肌肥大中的作用提供了新的认识。
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