کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2093682 1081973 2014 14 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
miR-133a Enhances the Protective Capacity of Cardiac Progenitors Cells after Myocardial Infarction
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیوتکنولوژی یا زیست‌فناوری
پیش نمایش صفحه اول مقاله
miR-133a Enhances the Protective Capacity of Cardiac Progenitors Cells after Myocardial Infarction
چکیده انگلیسی


• miR-1 and miR-133a have a role in adult cardiac progenitor cells (CPCs)
• miR-133a-CPCs protect cardiac function
• miR-133a-CPCs increase vascularization and protect against hypertrophy
• miR-133a is enriched in CPCs-derived exosomes

SummarymiR-133a and miR-1 are known as muscle-specific microRNAs that are involved in cardiac development and pathophysiology. We have shown that both miR-1 and miR-133a are early and progressively upregulated during in vitro cardiac differentiation of adult cardiac progenitor cells (CPCs), but only miR-133a expression was enhanced under in vitro oxidative stress. miR-1 was demonstrated to favor differentiation of CPCs, whereas miR-133a overexpression protected CPCs against cell death, targeting, among others, the proapoptotic genes Bim and Bmf. miR-133a-CPCs clearly improved cardiac function in a rat myocardial infarction model by reducing fibrosis and hypertrophy and increasing vascularization and cardiomyocyte proliferation. The beneficial effects of miR-133a-CPCs seem to correlate with the upregulated expression of several relevant paracrine factors and the plausible cooperative secretion of miR-133a via exosomal transport. Finally, an in vitro heart muscle model confirmed the antiapoptotic effects of miR-133a-CPCs, favoring the structuration and contractile functionality of the artificial tissue.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: - Volume 3, Issue 6, 9 December 2014, Pages 1029–1042
نویسندگان
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