کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10431855 | 910228 | 2014 | 25 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
HIP-55 negatively regulates myocardial contractility at the single-cell level
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کلمات کلیدی
موضوعات مرتبط
مهندسی و علوم پایه
سایر رشته های مهندسی
مهندسی پزشکی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Biomechanics - Volume 47, Issue 11, 22 August 2014, Pages 2715-2720
Journal: Journal of Biomechanics - Volume 47, Issue 11, 22 August 2014, Pages 2715-2720
نویسندگان
Rui Xing, Shanshan Li, Kai Liu, Yuan Yuan, Qing Li, Hao Deng, Chengzhi Yang, Jianyong Huang, Youyi Zhang, Jing Fang, Chunyang Xiong, Zijian Li,