کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8337857 | 1540969 | 2018 | 28 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Vitamin D attenuates pressure overload-induced cardiac remodeling and dysfunction in mice
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کلمات کلیدی
Left ventricular internal dimensionVDRWGAβ-MHCLVIDGRP78LVPWBNPIRE-1UPRATF-6TACANPSarcoplasmic/endoplasmic reticulum Ca2+ ATPase1,25-dihydroxyvitamin D - 1،25-دی هیدروکسوییتامین DC/EBP homologous protein - C / EBP پروتئین همولوگNADPH oxidases - NADPH اکسیدازNOx - NOXPKR-like ER kinase - PK-like ER kinaseER stress - استرس استCardiac remodeling - بازسازی قلبPressure overload - بیش از حد فشارtransverse aortic constriction - تنگی عرضی آئورتCHOP - تکه کردنDihydroethidine - دی هیدروتیدینβ-myosin heavy chain - زنجیره سنگین بتا-میوزینendoplasmic reticulum - شبکه آندوپلاسمی Left ventricular posterior wall thickness - ضخامت دیواره خلفی بطن چپtibia length - طول تیبیاactivating transcription factor 6 - فعال کردن عامل رونویسی 6SERCA - قلبSignaling pathways - مسیرهای سیگنالینگheart failure - نارسایی قلبیDHE - وbody weight - وزن بدنHeart weight - وزن قلبVitamin D - ویتامین دیUnfolded protein response - پاسخ پروتئین آشکارPERK - پرکbrain natriuretic peptide - پپتید ناتریورتیک مغزیatrial natriuretic peptide - پپتید نایروئیدوری دهلیزejection fraction - کسری خروجیfractional shortening - کوتاه کردن کسریWheat germ agglutinin - گیاه گندم آگلوتیینینVitamin D receptor - گیرنده ویتامین D
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Vitamin D (VD) and its analogues play critical roles in metabolic and cardiovascular diseases. Recent studies have demonstrated that VD exerts a protective role in cardiovascular diseases. However, the beneficial effect of VD on pressure overload-induced cardiac remodeling and dysfunction and its underlying mechanisms are not fully elucidated. In this study, cardiac dysfunction and hypertrophic remodeling in mice were induced by pressure overload. Cardiac function was evaluated by echocardiography, and myocardial histology was detected by H&E and Masson's trichrome staining. Cardiomyocyte size was detected by wheat germ agglutinin staining. The protein levels of signaling mediators were examined by western blotting while mRNA expression of hypertrophic and fibrotic markers was examined by qPCR analysis. Oxidative stress was detected by dihydroethidine staining. Our results showed that administration of VD3 significantly ameliorates pressure overload-induced contractile dysfunction, cardiac hypertrophy, fibrosis and inflammation in mice. In addition, VD3 treatment also markedly inhibited cardiac oxidative stress and apoptosis. Moreover, protein levels of calcineurin A, ERK1/2, AKT, TGF-β, GRP78, cATF6, and CHOP were significantly reduced whereas SERCA2 level was upregulated in the VD3-treated hearts compared with control. These results suggest that VD3 attenuates cardiac remodeling and dysfunction induced by pressure overload, and this protective effect is associated with inhibition of multiple signaling pathways.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The Journal of Steroid Biochemistry and Molecular Biology - Volume 178, April 2018, Pages 293-302
Journal: The Journal of Steroid Biochemistry and Molecular Biology - Volume 178, April 2018, Pages 293-302
نویسندگان
Liang Zhang, Xiao Yan, Yun-Long Zhang, Jie Bai, Tesfaldet Habtemariam Hidru, Qing-Shan Wang, Hui-Hua Li,