کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8839988 | 1613792 | 2016 | 23 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
MiR-195 dependent roles of mitofusin2 in the mitochondrial dysfunction of hippocampal neurons in SAMP8 mice
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: MiR-195 dependent roles of mitofusin2 in the mitochondrial dysfunction of hippocampal neurons in SAMP8 mice MiR-195 dependent roles of mitofusin2 in the mitochondrial dysfunction of hippocampal neurons in SAMP8 mice](/preview/png/8839988.png)
چکیده انگلیسی
Abnormal gene expression, including mRNAs, and microRNAs (miRNA), have been identified in the development of Alzheimer's disease (AD). Although mitofusin2 (mfn2) has been found to be down-regulated in the neurons from hippocampus and cortex in AD patients, little is known about its roles and the regulatory mechanisms in the pathogenesis of AD. This study was performed to investigate the roles of mfn2 protein and its upstream regulatory mechanism in the progression of AD using a senescence accelerated mouse prone-8 (SAMP8) model. The results of quantitative real-time PCR and western blot revealed that mfn2 expression displayed a consistent decrease with aging in the hippocampus of SAMP8 than did age-matched SAMR1 mice. The luciferase activity assay combined with mutational analysis confirmed the binding site of miR-195 to the 3â² -untranslated region (3â²-UTR) of mfn2 mRNA. Furthermore, miR-195 inhibitor or antigomir induced the higher level expression of mfn2 protein in vitro and in vivo. In addition, exogenous expression of miR-195 decreased the mitochondrial membrane potential (MMP) of the HT-22 cells by targeting mfn2. In conclusion, these results indicated that deregulation of mfn2 might be involved in mitochondrial dysfunction during the progression of AD, and its decreased expression was regulated at least in part by miR-195 in AD mice. The abnormal expression of miR-195 played a potential role in mitochondrial disorder by targeting mfn2 in hippocampus of SAMP8 mice. Therefore, upregulation of mfn2 protein by inhibiting miR-195 might be a potential new therapeutic strategy for treatment of AD.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research - Volume 1652, 1 December 2016, Pages 135-143
Journal: Brain Research - Volume 1652, 1 December 2016, Pages 135-143
نویسندگان
Rui Zhang, Huimin Zhou, Lei Jiang, Yueran Mao, Ximing Cui, Bing Xie, Dongsheng Cui, Hui Wang, Qingfu Zhang, Shunjiang Xu,