MicroRNA-127 targeting of mitoNEET inhibits neurite outgrowth, induces cell apoptosis and contributes to physiological dysfunction after spinal cord transection

نویسندگان

  • Qin-Qin He
  • Liu-Lin Xiong
  • Fei Liu
  • Xiang He
  • Guo-Ying Feng
  • Fei-Fei Shang
  • Qing-Jie Xia
  • You-Cui Wang
  • De-Lu Qiu
  • Chao-Zhi Luo
  • Jia Liu
  • Ting-Hua Wang
چکیده

Neuroregeneration and apoptosis are two important pathophysiologic changes after spinal cord injury (SCI), but their underlying mechanisms remain unclear. MicroRNAs (miRNAs) play a crucial role in the regulation of neuroregeneration and neuronal apoptosis, research areas that have been greatly expanded in recent years. Here, using miRNA arrays to profile miRNA transcriptomes, we demonstrated that miR-127-3p was significantly down-regulated after spinal cord transection (SCT). Then, bioinformatics analyses and experimental detection showed that miR-127-3p exhibited specific effects on the regulation of neurite outgrowth and the induction of neuronal apoptosis by regulating the expression of the mitochondrial membrane protein mitoNEET. Moreover, knockdown of MitoNEET leaded to neuronal loss and apoptosis in primary cultured spinal neurons. This study therefore revealed that miR-127-3p, which targets mitoNEET, plays a vital role in regulating neurite outgrowth and neuronal apoptosis after SCT. Thus, modificatioin of the mitoNEET expression, such as mitoNEET activition may provide a new strategy for the treatment of SCI in preclinical trials.

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Erratum: MicroRNA-127 targeting of mitoNEET inhibits neurite outgrowth, induces cell apoptosis and contributes to physiological dysfunction after spinal cord transection

“We thank Dr. Zhi-cheng Xiao for discussion and critical comments, Dr. Visar for close editing of the manuscript. This research was supported by a Grant of National Science Foundation of China, No. 81271358, and a Grant of National Science Foundation of China, No. 81271358, and a Grant of National Science Foundation of China, No. 81471268. This study was also supported by the Program for IRTSTY...

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عنوان ژورنال:

دوره 6  شماره 

صفحات  -

تاریخ انتشار 2016