HIP-55 negatively regulates myocardial contractility at the single-cell level |
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| Authors: | Rui Xing Shanshan Li Kai Liu Yuan Yuan Qing Li Hao Deng Chengzhi Yang Jianyong Huang Youyi Zhang Jing Fang Chunyang Xiong Zijian Li |
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| Institution: | 1. Institute of Vascular Medicine, Peking University Third Hospital, Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Ministry of Health, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education and Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing, China;2. Academy for Advanced Interdisciplinary Studies, Peking University, Beijing, China;3. College of Engineering, Peking University, Beijing, China |
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| Abstract: | Myocardial contractility is crucial for cardiac output and heart function. But the detailed mechanisms of regulation remain unclear. In the present study, we found that HIP-55, an actin binding protein, negatively regulates myocardial contractility at the single-cell level. HIP-55 was overexpressed and knocked down in cardiomyocytes with an adenovirus infection. The traction forces exerted by single cardiomyocyte were measured using cell traction force microscopy. The results showed that HIP-55 knockdown significantly increased the contractility of the cardiomyocytes and HIP-55 overexpression could markedly reverse this process. Furthermore, HIP-55 was obviously co-localized with F-actin in cardiomyocytes, suggesting that HIP-55 regulated cardiac contractile function through the interaction between HIP-55 and F-actin. This study reveals the regulatory mechanisms of myocardial contractility and provides a new target for preventing and treating cardiovascular disease. |
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| Keywords: | HIP-55 Myocardial contractility Traction force microscopy |
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