کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8322121 | 1539847 | 2018 | 32 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
MiR-34a regulates mitochondrial content and fat ectopic deposition induced by resistin through the AMPK/PPARα pathway in HepG2 cells
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Resistin is an adipocyte-derived cytokine and was named for its role in the development of insulin resistance. Increased serum resistin levels are also associated with steatohepatitis and non-alcoholic fatty liver disease. In a previous study, resistin was observed to reduce mitochondrial content and upregulate miR-34a significantly in the liver. In this study, male C57BL/6 mice were injected with agomir-34a or control agomir, and HepG2 cells were transfected with miR-34a mimics or inhibitors to assess their role in resistin-induced fat deposition. The overexpression of miR-34a increased liver and HepG2 cell TAG content, decreased mitochondrial content, changed mitochondrial morphology and impaired mitochondrial function. In contrast, a miR-34a inhibitor significantly restored the TAG content and mitochondrial transmembrane potential. A study of transcriptional regulation revealed that C/EBPβ is essential for upregulating miR-34a by resistin. Furthermore, miR-34a inhibited the PPARα signaling pathway by binding to sites in the 3â²UTR of AdipoR2 genes and the AMPK pathway. Consequently, this increased the fat content and decreased the mitochondrial content in HepG2 cells. This paper reveals a novel mechanism for mitochondrial regulation, which suggests that normal mitochondrial content and function is crucial for lipid metabolism in the liver.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The International Journal of Biochemistry & Cell Biology - Volume 94, January 2018, Pages 133-145
Journal: The International Journal of Biochemistry & Cell Biology - Volume 94, January 2018, Pages 133-145
نویسندگان
Fengyun Wen, Chaoqing An, Xiaotian Wu, Yi Yang, Jingjing Xu, Yasong Liu, Chunming Wang, Leitong Nie, Hubin Fang, Zaiqing Yang,