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6. VIRMA promotes neuron apoptosis via inducing m6A methylation of STK10 in spinal cord injury animal models.

Author

Hong, Hongxiang, Xu, Guanhua, Bao, Guofeng, Zhang, Jinlong, Chen, Chu, Chen, Jiajia, Wu, Chunshuai, Jiang, Jiawei, Huang, Jiayi, Huang, Haiming, and Cui, Zhiming

Subjects
*SPINAL cord injuries, *METHYLATION, *ANIMAL models in research, *APOPTOSIS, *NEURONS, *CELL death
Abstract

Background: Spinal cord injury (SCI) occurs as a devastating neuropathic disease. The role of serine–threonine kinase 10 (STK10) in the development of SCI remains unclear. Objective: This study aimed to investigate the action of m6A methylation on STK10 in the apoptosis of spinal cord neurons in the pathogenesis of SCI and the possible underlying mechanisms. Methods: Rat model of SCI was established and subsequently evaluated for motor function, pathological conditions, and apoptosis of spinal cord neurons. And the effects of overexpression of STK10 on neuronal cells in animal models of spinal cord injury and glyoxylate deprivation (OGD) cell models were evaluated. m6A2Target database and SRAMP database were used to predict the m6A methylation sites of STK10. The methylation kits were used to detect overall m6A methylation. Finally, the interaction between STK10 and vir like m6A methyltransferase associated (VIRMA) was explored in animal and cellular models. Results: STK10 is markedly decreased in spinal cord injury models and overexpression of STK10 inhibits neuronal apoptosis. VIRMA can induce m6A methylation of STK10. VIRMA is over‐expressed in spinal cord injury models and negatively regulates the expression of STK10. m6A methylation and apoptosis of neuronal cells are reduced by the knockdown of VIRMA and STK10 shRNA have shown the opposite effects. Conclusions: VIRMA promotes neuronal apoptosis in spinal cord injury by regulating STK10 m6A methylation. [ABSTRACT FROM AUTHOR]

Published
2024
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12. Ubiquitin ligase Triad1 promotes neurite outgrowth by inhibiting MDM2-mediated ubiquitination of the neuroprotective factor pleiotrophin

Author

Wu, Chunshuai, primary, Xu, Guanhua, additional, Bao, Guofeng, additional, Gao, Hong, additional, Chen, Jiajia, additional, Zhang, Jinlong, additional, Chen, Chu, additional, Hong, Hongxiang, additional, Xue, Pengfei, additional, Jiang, Jiawei, additional, Liu, Yang, additional, Huang, Jiayi, additional, Sun, Yue, additional, Fu, Jiawei, additional, Li, Yiqiu, additional, and Cui, Zhiming, additional

Published
2022
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18. Can zinc protect cells from the cytotoxic effects of cobalt ions and nanoparticles derived from metal-on-metal joint arthroplasties?

Author

Fan Liu, Wei Wang, Hong Hongxiang, Yake Liu, and Huijun Zhu

Subjects
0301 basic medicine, chemistry.chemical_element, Nanoparticle, 02 engineering and technology, Zinc, COBALT TOXICITY, Metal, 03 medical and health sciences, Cobalt Nanoparticles, Protective Effects, Orthopedics and Sports Medicine, Research, Cobalt Ions, 021001 nanoscience & nanotechnology, 030104 developmental biology, chemistry, visual_art, visual_art.visual_art_medium, Cobalt ions, Surgery, Cobalt Cytotoxicity, 0210 nano-technology, Cobalt, Nuclear chemistry
Abstract

Objectives Recently, high failure rates of metal-on-metal (MOM) hip implants have raised concerns of cobalt toxicity. Adverse reactions occur to cobalt nanoparticles (CoNPs) and cobalt ions (Co2+) during wear of MOM hip implants, but the toxic mechanism is not clear. Methods To evaluate the protective effect of zinc ions (Zn2+), Balb/3T3 mouse fibroblast cells were pretreated with 50 μM Zn2+ for four hours. The cells were then exposed to different concentrations of CoNPs and Co2+ for four hours, 24 hours and 48 hours. The cell viabilities, reactive oxygen species (ROS) levels, and inflammatory cytokines were measured. Results CoNPs and Co2+ can induce the increase of ROS and inflammatory cytokines, such as tumour necrosis factor α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6). However, Zn pretreatment can significantly prevent cytotoxicity induced by CoNPs and Co2+, decrease ROS production, and decrease levels of inflammatory cytokines in Balb/3T3 mouse fibroblast cells. Conclusion These results suggest that Zn pretreatment can provide protection against inflammation and cytotoxicity induced by CoNPs and Co2+ in Balb/3T3 cells. Cite this article: Y. Liu, H. Zhu, H. Hong, W. Wang, F. Liu. Can zinc protect cells from the cytotoxic effects of cobalt ions and nanoparticles derived from metal-on-metal joint arthroplasties? Bone Joint Res 2017;6:649–655. DOI: 10.1302/2046-3758.612.BJR-2016-0137.R2.

Published
2017

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