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Iranian Journal of Basic Medical Sciences، جلد ۲۵، شماره ۸، صفحات ۹۶۴-۹۶۹
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عنوان انگلیسی LOXL2 silencing suppresses angiotensin II-induced cardiac hypertrophy through the EMT process and TGF-β1/Smad3/NF-κB pathway
چکیده انگلیسی مقاله Objective(s): Atrial fibrillation (AF) is a common arrhythmia with atrial myocyte hypertrophy linked with stroke, heart failure, and increased mortality. Lysyl oxidase-like 2 (LOXL2) involves the cross-linking of collagen in the extracellular matrix (ECM). In the present study, we investigated the roles and underlying mechanisms of LOXL2 on cardiomyocyte hypertrophy. Materials and Methods: The expression of LOXL2 mRNA and protein were detected in angiotensin II (Ang II) treated rat cardiomyocytes H9c2 by RT-qPCR and western blot. Small interfering RNA (siRNA) mediated LOXL2 gene silencing was used to evaluate cardiac hypertrophy and related markers. Also, the protein expression of EMT markers and Smad3/NF-κB pathway was determined by western blot. Results: Ang II significantly increased mRNA and protein expressions of LOXL2 and increased mRNA levels of myocardial hypertrophy markers, including ANP, BNP, and β-MHC in H9c2 cells. Silencing of LOXL2 significantly suppressed Ang II-induced hypertrophy and reversed the increase in ANP, BNP, and β-MHC mRNA levels. Also, EMT markers’ expressions, as evidenced by increased E-cadherin and decreased vimentin, α-smooth muscle actin (α-SMA), fibroblast-specific protein (FSP), and collagen 1A1. Mechanistically, we found that LOXL2 silencing suppressed protein expressions of TGF-β1, p-Smad3, and p-NF-κB in Ang II-stimulated H9c2 cells. LOXL2 silencing also attenuated Ang II-induced increased expression and content of proinflammatory cytokines IL-1β (H) and TNF-α. Conclusion: Our data speculated that LOXL2 might be a potential contributing factor to Ang II-induced cardiac hypertrophy, and TGF-β1/Smad3/NF-κB is involved in a signal axis and might be a potential strategy in treating cardiac hypertrophy. 
کلیدواژه‌های انگلیسی مقاله Angiotensin II, Atrial fibrillation, Epithelial-mesenchymal - transition, Hypertrophy, LOXL2 protein
نویسندگان مقاله | Jun Luo
Department of Cardiology, Shanghai University of Medicine & Health Sciences affiliated Zhoupu Hospital, Shanghai 201318, China


| Yingbiao Wu
Department of Cardiology, Shanghai University of Medicine & Health Sciences affiliated Zhoupu Hospital, Shanghai 201318, China


| Xi Zhu
Department of Cardiology, Shanghai University of Medicine & Health Sciences affiliated Zhoupu Hospital, Shanghai 201318, China


| Saihua Wang
Department of Cardiology, Shanghai University of Medicine & Health Sciences affiliated Zhoupu Hospital, Shanghai 201318, China


| Xiaogang Zhang
Department of Cardiology, Shanghai University of Medicine & Health Sciences affiliated Zhoupu Hospital, Shanghai 201318, China


| Zhongping Ning
Department of Cardiology, Shanghai University of Medicine & Health Sciences affiliated Zhoupu Hospital, Shanghai 201318, China
نشانی اینترنتی https://ijbms.mums.ac.ir/article_20824.html
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