Issue
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.
Knockdown of JMJD1C, a target gene of hsa-miR-590-3p, inhibits mitochondrial dysfunction and oxidative stress in MPP+-treated MES23.5 and SH-SY5Y cells
Corresponding Author(s) : J Wang
jinlanwangedu@163.com
Cellular and Molecular Biology,
Vol. 62 No. 3: Issue 3
Abstract
MicroRNAs have been shown to be closely related to many neurodegenerative disorders. The present study focuses on the role of hsa-miR-590-3p and its function in Parkinson's disease (PD). Our study showed a remarkable down-regulation of miR-590-3p expression in the 1-methyl-4 phenylpyridinium (MPP+)-treated MES23.5 and SH-SY5Y cells. Furthermore, JMJD1C was identified as a target gene of miR-590-3p in humans via the luciferase reporter assay. Our study also demonstrated that up-regulation of miR-590-3p and knockdown of JMJD1C increased the expression of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) and the downstream targets of PGC-1α, including nuclear respiratory factor 1 (NRF-1) and mitochondrial transcription factor A (TFAM), which are the key genes regulating mitochondrial function. Also, the expression of heme oxygenase-1 (HO-1), NAD (P) H quinone oxidoreductase-1 (NQO-1) and γ-glutamylcysteine synthetase (γ-GCS) involved in anti-oxidation was increased. Moreover, there was a significant increase in the total cellular ATP with an associated decrease in levels of ROS in the absence of JMJD1C. Taken together, these results show that miR-590-3p plays an important role in the pathogenesis of PD, which may be further regarded as a therapeutic target.
Keywords
Parkinson's disease
hsa-miR-590-3p
JMJD1C
mitochondrial functions
oxidative stress.
Wang, J., Le, T., Wei, R., & Jiao, Y. (2016). Knockdown of JMJD1C, a target gene of hsa-miR-590-3p, inhibits mitochondrial dysfunction and oxidative stress in MPP+-treated MES23.5 and SH-SY5Y cells. Cellular and Molecular Biology, 62(3), 39–45. Retrieved from http://mail.cellmolbiol.org/index.php/CMB/article/view/818
Download Citation
Endnote/Zotero/Mendeley (RIS)BibTeX