| 丝氨酸蛋白酶Omi/HtrA2表达增加促进心肌衰老的作用 |
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| 引用本文： | 丝氨酸蛋白酶Omi/HtrA表达增加促进心肌衰老的作用. 丝氨酸蛋白酶Omi/HtrA2表达增加促进心肌衰老的作用[J]. 首都医科大学学报, 2021, 42(5): 783-789. DOI: 10.3969/j.issn.1006-7795.2021.05.014 |
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| 作者姓名： | 丝氨酸蛋白酶Omi/HtrA表达增加促进心肌衰老的作用 |
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| 作者单位： | 首都医科大学基础医学院生理学与病理生理学系,北京 100069;代谢紊乱相关心血管疾病北京市重点实验室,北京100069;首都医科大学燕京医学院,北京101300;首都医科大学基础医学院生理学与病理生理学系,北京 100069;代谢紊乱相关心血管疾病北京市重点实验室,北京100069;首都医科大学燕京医学院,北京101300 |
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| 基金项目： | 国家自然科学基金;北京市自然科学基金;首都医科大学燕京医学院学院基金 |
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| 摘 要： | 目的 观察线粒体促凋亡蛋白Omi/HtrA2表达增加对心肌衰老的影响。方法 构建心肌特异性过表达Omi/HtrA2小鼠模型,通过Western blotting法检测衰老标志物p53、p21、p16表达水平;分析Omi/HtrA2与衰老标志物表达的相关性;构建Omi/HtrA2稳转H9c2细胞系,通过Western blotting法检测Omi/HtrA2表达增加后衰老指标p53、p21、p16的改变;通过β-半乳糖苷酶(β-gal)染色比较β-半乳糖苷酶染色阳性衰老细胞的改变;通过Omi/HtrA2特异性抑制剂UCF101抑制Omi/HtrA2功能,检测抑制Omi/HtrA2活性后衰老标志物的表达水平及阳性衰老细胞变化。结果 (1)与对照组相比,心肌特异性过表达Omi/HtrA2小鼠心肌组织中,Omi/HtrA2表达量显著增加(P<0.01);过表达Omi/HtrA2心肌组织衰老标志物p53、p21、p16增加(P<0.01);(2)在心肌组织中Omi/HtrA2表达量与衰老标志物p53、p21、p16呈正相关(P<0.05);(3)与H9c2细胞(control组)相比,Omi/HtrA2稳转H9c2细胞(Omi组)衰老标志物p53、p21、p16表达增加(P<0.05);β-半乳糖苷酶染色结果显示,Omi组衰老细胞增加;与Omi组相比,Omi/HtrA2特异性抑制剂UCF101处理组(Omi+UCF101组)衰老标志物p53、p21、p16表达降低(P<0.05);β-半乳糖苷酶染色阳性细胞减少。结论 Omi/HtrA2的表达与衰老标志物呈正相关,表达增加的Omi/HtrA2促进心肌衰老。
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| 关 键 词： | Omi/HtrA2 心肌 衰老 |
| 收稿时间： | 2021-01-11 |
Omi/HtrA2 overexpression is associated with myocardial aging |
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| Wei Xin,Liu Dan,Wu Ye,Lyu Kunyi,Shen Yan,Liu Huirong. Omi/HtrA2 overexpression is associated with myocardial aging[J]. Journal of Capital Medical University, 2021, 42(5): 783-789. DOI: 10.3969/j.issn.1006-7795.2021.05.014 |
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| Authors: | Wei Xin Liu Dan Wu Ye Lyu Kunyi Shen Yan Liu Huirong |
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| Affiliation: | 1. Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China; 2. Beijing Key Laboratory of Metabolic Disturbance Related Cardiovascular Disease, Beijing 100069, China; 3. Yan Jing Medical College, Capital Medical University, Beijing 101300, China |
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| Abstract: | Objective To observe the effect of increased serine protease Omi/HtrA2 on myocardial aging. Methods Overexpressed cardiac-specific Omi/HtrA2 transgenic mice was constructed, the expression of senescence markers p53, p21 and p16 were detected by Western blotting, and the correlation between Omi/HtrA2 and the senescence markers was analyzed. The aging indicators were detected in overexpressed Omi/HtrA2 H9c2 cells (Omi group) by Western blotting. The senescent cells were detected by β-galactosidase staining. Compared with overexpressed Omi/HtrA2 cells, the expression of senescence markers and the β-galactosidase positive senescent cells were detected after inhibiting the function of Omi/HtrA2 by Omi/HtrA2 specific inhibitor UCF101. Results (1) Compared with the control group, the expression of Omi/HtrA2 was significantly increased in the heart of myocardium-specific overexpressed Omi/HtrA2 transgenic mice (P<0.01). The aging markers p53, p21 and p16 were significantly increased in Omi/HtrA2 overexpressed group(P<0.01). (2) The expression of Omi/HtrA2 was positively correlated with the aging markers p53, p21, and p16 (P<0.01). (3) Compared with H9c2 cells (control group), expression of the senescence markers p53, p21 and p16 and the β-galactosidase positive senescent cells increased in Omi group (P<0.05). Compared with Omi group, expression of the senescence markers and the β-galactosidase positive senescent cells decreased in Omi/HtrA2 H9c2 cells treated by Omi/HtrA2 specific inhibitor UCF101 (Omi+UCF101 group) (P<0.05). Conclusion The expression of Omi/HtrA2 is positively correlated with aging markers. Overexpression of Omi/HtrA2 promoted myocardial aging. |
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| Keywords: | Omi/HtrA2 myocardium aging |
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