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

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 expan...

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Autores principales: He, Qin-Qin, Xiong, Liu-Lin, Liu, Fei, He, Xiang, Feng, Guo-Ying, Shang, Fei-Fei, Xia, Qing-Jie, Wang, You-Cui, Qiu, De-Lu, Luo, Chao-Zhi, Liu, Jia, Wang, Ting-Hua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5066253/
https://www.ncbi.nlm.nih.gov/pubmed/27748416
http://dx.doi.org/10.1038/srep35205
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author He, Qin-Qin
Xiong, Liu-Lin
Liu, Fei
He, Xiang
Feng, Guo-Ying
Shang, Fei-Fei
Xia, Qing-Jie
Wang, You-Cui
Qiu, De-Lu
Luo, Chao-Zhi
Liu, Jia
Wang, Ting-Hua
author_facet He, Qin-Qin
Xiong, Liu-Lin
Liu, Fei
He, Xiang
Feng, Guo-Ying
Shang, Fei-Fei
Xia, Qing-Jie
Wang, You-Cui
Qiu, De-Lu
Luo, Chao-Zhi
Liu, Jia
Wang, Ting-Hua
author_sort He, Qin-Qin
collection PubMed
description 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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spelling pubmed-50662532016-10-26 MicroRNA-127 targeting of mitoNEET inhibits neurite outgrowth, induces cell apoptosis and contributes to physiological dysfunction after spinal cord transection He, Qin-Qin Xiong, Liu-Lin Liu, Fei He, Xiang Feng, Guo-Ying Shang, Fei-Fei Xia, Qing-Jie Wang, You-Cui Qiu, De-Lu Luo, Chao-Zhi Liu, Jia Wang, Ting-Hua Sci Rep Article 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. Nature Publishing Group 2016-10-17 /pmc/articles/PMC5066253/ /pubmed/27748416 http://dx.doi.org/10.1038/srep35205 Text en Copyright © 2016, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Article
He, Qin-Qin
Xiong, Liu-Lin
Liu, Fei
He, Xiang
Feng, Guo-Ying
Shang, Fei-Fei
Xia, Qing-Jie
Wang, You-Cui
Qiu, De-Lu
Luo, Chao-Zhi
Liu, Jia
Wang, Ting-Hua
MicroRNA-127 targeting of mitoNEET inhibits neurite outgrowth, induces cell apoptosis and contributes to physiological dysfunction after spinal cord transection
title MicroRNA-127 targeting of mitoNEET inhibits neurite outgrowth, induces cell apoptosis and contributes to physiological dysfunction after spinal cord transection
title_full MicroRNA-127 targeting of mitoNEET inhibits neurite outgrowth, induces cell apoptosis and contributes to physiological dysfunction after spinal cord transection
title_fullStr MicroRNA-127 targeting of mitoNEET inhibits neurite outgrowth, induces cell apoptosis and contributes to physiological dysfunction after spinal cord transection
title_full_unstemmed MicroRNA-127 targeting of mitoNEET inhibits neurite outgrowth, induces cell apoptosis and contributes to physiological dysfunction after spinal cord transection
title_short MicroRNA-127 targeting of mitoNEET inhibits neurite outgrowth, induces cell apoptosis and contributes to physiological dysfunction after spinal cord transection
title_sort microrna-127 targeting of mitoneet inhibits neurite outgrowth, induces cell apoptosis and contributes to physiological dysfunction after spinal cord transection
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5066253/
https://www.ncbi.nlm.nih.gov/pubmed/27748416
http://dx.doi.org/10.1038/srep35205
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