کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10953714 | 1097764 | 2015 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Volume overload induces autophagic degradation of procollagen in cardiac fibroblasts
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کلمات کلیدی
CM-DCFECMTGFACFDMNQLVEDdLVESDTissue inhibitor of MMPTNFMMPROS - ROSAutophagy - اتوفاژیVolume overload - اضافه بار دورهTem - این استLeft ventricular - بطن چپPressure overload - بیش از حد فشارtransforming growth factor - تبدیل فاکتور رشدOxidative stress - تنش اکسیداتیوTIMP - زمانendoplasmic reticulum - شبکه آندوپلاسمی tumor necrosis factor - فاکتور نکروز تومورCardiac fibroblast - فیبروبلاست قلبAortocaval fistula - فیستول AortocavilleExtracellular matrix - ماتریکس خارج سلولیmatrix metalloproteinase - ماتریکس متالوپروتئینازTransmission electron microscopy - میکروسکوپ الکترونی عبوریmitral regurgitation - نارسایی میترالfractional shortening - کوتاه کردن کسریReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
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چکیده انگلیسی
In a pure volume overloaded (VO) heart, interstitial collagen loss is degraded by matrix metalloproteinases (MMPs) that leads to left ventricular (LV) dilatation and heart failure. Cardiac fibroblasts are the primary source of extracellular matrix proteins that connect cardiomyocytes. The goal of this study was to determine how VO affects intracellular procollagen in cardiac fibroblasts. Using the aortocaval fistula (ACF) model in Sprague-Dawley rats, we demonstrate that cardiac fibroblasts isolated from 4 and 12Â wk ACF animals have decreased intracellular procollagen I compared to the fibroblasts from age-matched shams. The reduction of procollagen I is associated with increased autophagy as demonstrated by increased autophagic vacuoles and LC3-II expression. To test the relationship between autophagy and procollagen degradation, we treated adult cardiac fibroblasts with either an autophagy inducer, rapamycin, or an inhibitor, wortmannin, and found that procollagen I protein levels were decreased in fibroblasts treated with rapamycin and elevated in wortmannin-treated cells. In addition, we demonstrated that VO induces oxidative stresses in cardiac fibroblasts from 4 and 12Â wk ACF rats. Treatment of cultured cardiac fibroblasts with an oxidative stress-inducing agent (DMNQ) induces autophagy and intracellular procollagen I and fibronectin degradation, which is reversed by wortmannin but not by the global MMP inhibitor (PD166793). Mechanical stretch of cardiac fibroblasts also induces oxidative stress and autophagic degradation of procollagen I and fibronectin. Our results suggest that in addition to the well-known effects of MMPs on extracellular collagen degradation in VO, there is a concurrent degradation of intracellular procollagen and fibronectin mediated by oxidative stress-induced autophagy in cardiac fibroblasts.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 89, Part B, December 2015, Pages 241-250
Journal: Journal of Molecular and Cellular Cardiology - Volume 89, Part B, December 2015, Pages 241-250
نویسندگان
Lianwu Fu, Chih-Chang Wei, Pamela C. Powell, Wayne E. Bradley, James F. Collawn, Louis J. Dell'Italia,