
氯离子通道蛋白1在心肌纤维化进程中的表达特征
Expression of anoctamin 1 in the process of myocardial fibrosis
目的 探讨氯离子通道蛋白1(ANO1)在心肌纤维化进程中的表达特征,为抑制心肌纤维化寻找新的靶点。 方法 采用冠状动脉结扎法制作大鼠心肌梗死模型,1周后取心肌梗死组和假手术组大鼠左心室组织,采用免疫组织化学染色、免疫荧光双标记检测梗死区和正常组织ANO1表达的变化;体外分离培养心肌成纤维细胞,采用免疫荧光标记、Real-time PCR和Western blotting检测心肌成纤维细胞中ANO1表达情况。 结果 制造模型1周后心肌梗死区ANO1表达明显增强,并与α-平滑肌肌动蛋白(α-SMA)共表达;ANO1蛋白明显表达于心肌成纤维细胞的核膜和胞质中,且表达强度和α-SMA具有相同的趋势;与刚分离贴壁心肌纤维细胞相比,ANO1在培养和48 h后的心肌成纤维细胞中表达量明显增强。 结论 ANO1在心肌成纤维细胞转化为成肌纤维细胞过程中表达量增加,提示ANO1可能在心肌纤维化进程中发挥重要调控作用。
Objective To clarify the expression feature of anoctamin 1(ANO1) in the process of cardiac fibrosis and seek new targets for preventing it. Methods The myocardial infarction (MI) rats were prepared by coronary artery ligation. The left ventricular from MI group and the sham operation group were taken at one week (1 week) after MI. The changes of ANO1 expression in the two groups were detected by immunohistochemical staining and immunofluorescence double labeling. The expression of ANO1 in cardiac fibroblasts (CFs) was detected by immunofluorescence labeling, Real-time PCR and Western blotting. Results ANO1 exhibited high expression in MI and co-expressed with α-smooth muscle actin(α-SMA), and it was clearly expressed in the nucleus membrane and cytoplasm of CFs. The expression intensity of ANO1 was coincident with α-SMA. Furthermore, ANO1 expression increased significantly in the CFs after 48 hours culture comparing with the new isolated CFs. Conclusion The expression of ANO1 enhances markedly during the transformation of CFs into myocardial fibroblasts, suggesting that ANO1 may play an important role in the process of cardiac fibrosis.
氯离子通道蛋白1 / 钙激活氯通道 / 心肌成纤维细胞 / 心肌纤维化 / 免疫组织化学 / 大鼠
Anoctamin1 / Calcium-activated chloride channels / Cardiac fibroblasts / Myocardial fibrosis / Immunohistochemistry / Rat
[16]Duvvuri U, Shiwarski DJ, Xiao D, et al. TMEM16A induces MAPK and contributes directly to tumorigenesis and cancer progression [J]. Cancer Res, 2012, 72 (13): 3270-3281.[
17]Wang M, Yang H, Zheng LY, et al. Downregulation of TMEM16A calciumactivated chloride channel contributes to cerebrovascular remodeling during hypertension by promoting basilar smooth muscle cell proliferation [J]. Circulation, 2012, 125 (5): 697-707.
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