کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8689815 | 1581068 | 2018 | 39 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Normalization of connexin 43 protein levels prevents cellular and functional signs of dystrophic cardiomyopathy in mice
ترجمه فارسی عنوان
عادی سازی سطح پروتئین کنکسین 43 مانع از نشانه های سلولی و عملکردی قلب و عروق کرونر در موش
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کلمات کلیدی
کانکسین، کاردیومیوپاتی، دیستروفی عضلانی دوون استرس اکسیداتیو، دست زدن به کلسیم،
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب تکاملی
چکیده انگلیسی
Duchenne muscular dystrophy (DMD) associated cardiomyopathy remains incurable. Connexin 43 (Cx43) is upregulated and remodeled in the hearts of mdx mice, a mouse model of DMD. Hearts from Wild Type, mdx, and mdx:Cx43(+/â) mice were studied before (4-6 months) and after (10-15 months) the onset of cardiomyopathy to assess the impact of decreasing Cx43 levels on cardiac pathology in dystrophic mice. Increased connexin 43 protein levels in mdx hearts were not observed in mdx:Cx43(+/â) hearts. Cx43 remodeling in mdx hearts was attenuated in mdx:Cx43(+/â) hearts. At time-point 4-6 months, isolated cardiomyocytes from mdx hearts displayed enhanced ethidium bromide uptake, augmented intracellular calcium signals and increased production of reactive oxygen species. These pathological features were improved in mdx:Cx43(+/â) cardiomyocytes. Isoproterenol-challenged mdx:Cx43(+/â) mice did not show arrhythmias or acute lethality observed in mdx mice. Likewise, isoproterenol-challenged mdx:Cx43(+/â) isolated hearts were also protected from arrhythmogenesis. At time-point 10-15 months, mdx:Cx43(+/â) mice showed decreased cardiac fibrosis and improved ventricular function, relative to mdx mice. These results suggest that normalization of connexin 43 protein levels in mdx mice reduces overall cardiac pathology.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuromuscular Disorders - Volume 28, Issue 4, April 2018, Pages 361-372
Journal: Neuromuscular Disorders - Volume 28, Issue 4, April 2018, Pages 361-372
نویسندگان
J. Patrick Gonzalez, Jayalakshmi Ramachandran, Eric Himelman, Myriam A. Badr, Chifei Kang, Julie Nouet, Nadezhda Fefelova, Lai-Hua Xie, Natalia Shirokova, Jorge E. Contreras, Diego Fraidenraich,