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JCR 2016
جستجوی مقالات
چهارشنبه 26 شهریور 1404
Iranian Journal of Basic Medical Sciences
، جلد ۲۵، شماره ۱۰، صفحات ۱۲۰۱-۱۲۰۶
عنوان فارسی
چکیده فارسی مقاله
کلیدواژههای فارسی مقاله
عنوان انگلیسی
Crim1 inhibits angiotensin II-induced hypertrophy and preserves Kv4.2 expression in cardiomyocytes
چکیده انگلیسی مقاله
Objective(s): Angiotensin II (Ang II) plays a key role in the regulation of myocardial hypertrophy via downstream cysteine-rich transmembrane bone morphogenetic protein regulator 1 (Crim1). However, it is still unclear whether Crim1 is involved in ionic channel remodeling. The study aimed to explore the effects of Crim1 on transient outward potassium current (Ito) and Kv4.2 (the main subunit of Ito channel) expression in hypertrophic ventricular cardiomyocytes. Materials and Methods: The ventricular cardiomyocytes were isolated from the neonatal rats. Hypertrophy was induced by Ang II. Crim1 expression was modulated by using adenovirus transfection. The expression of myosin heavy chain beta (β-MHC), Crim1, and Kv4.2 was determined by RT-qPCR and western blot. The cellular surface area was assessed using Image J software. Ito was recorded by the whole-cell patch clamp technique. Results: Ang II-induced hypertrophy in cardiomyocytes was identified by their larger cellular surface area and higher mRNA expression of β-MHC. Ang II significantly decreased the expression of Crim1 and Kv4.2 and reduced Ito current density. However, Crim1 overexpression abolished the Ang II-induced hypertrophy and preserved the expression of Kv4.2 and Ito current density. Conclusion: Crim1 overexpression inhibits Ang II-induced hypertrophy and preserves Ito current density via up-regulating Kv4.2 in ventricular cardiomyocytes from neonatal rats. Crim1 could have a role in the development of ventricular arrhythmia in hypertrophic hearts.
کلیدواژههای انگلیسی مقاله
Angiotensin II, Cysteine-rich transmembrane, bone morphogenetic protein - regulator 1, Ion channel remodeling, Transient outward - potassium current, Ventricular hypertrophy
نویسندگان مقاله
| Jionghong He
Department of Cardiology, Guizhou Provincial People’s Hospital, Guiyang 550002 China
| Guiling Xia
Department of Cardiology, Guizhou Provincial People’s Hospital, Guiyang 550002 China
| long yang
Department of Cardiology, Guizhou Provincial People’s Hospital, Guiyang 550002 China
| Zhi Jiang
Department of Cardiology, Guizhou Provincial People’s Hospital, Guiyang 550002 China
| Ying Yang
Department of Cardiology, Guizhou Provincial People’s Hospital, Guiyang 550002 China
| Zhaomei Huo
Department of Cardiology, Guizhou Provincial People’s Hospital, Guiyang 550002 China
| Chuxian Guo
Department of Cardiology, Guizhou Provincial People’s Hospital, Guiyang 550002 China
نشانی اینترنتی
https://ijbms.mums.ac.ir/article_21061.html
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Original Article
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