1. Academic Validation
  2. Transient receptor potential ankyrin 1 contributes to the lysophosphatidylcholine-induced oxidative stress and cytotoxicity in OLN-93 oligodendrocyte

Transient receptor potential ankyrin 1 contributes to the lysophosphatidylcholine-induced oxidative stress and cytotoxicity in OLN-93 oligodendrocyte

  • Cell Stress Chaperones. 2020 Nov;25(6):955-968. doi: 10.1007/s12192-020-01131-y.
Chao Tian 1 2 3 Shuai Li 1 3 Lang He 4 Xiaobo Han 1 3 Feng Tang 1 2 3 Rongqi Huang 1 3 Zuoxian Lin 1 3 Sihao Deng 5 Junjie Xu 2 Hualin Huang 1 3 Huifang Zhao 1 3 Zhiyuan Li 6 7 8 9 10
Affiliations

Affiliations

  • 1 Key Laboratory of Regenerative Biology, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, Guangdong, China.
  • 2 Guangzhou JYK Biotechnology Company Limited, Guangzhou, Guangdong, China.
  • 3 Guangzhou Regenerative Medicine and Health Guangdong Laboratory, Guangzhou, Guangdong, China.
  • 4 Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
  • 5 Department of Anatomy and Neurobiology, School of Basic Medical Sciences, Central South University, Changsha, Hunan, China.
  • 6 Key Laboratory of Regenerative Biology, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, Guangdong, China. [email protected].
  • 7 Department of Anatomy and Neurobiology, School of Basic Medical Sciences, Central South University, Changsha, Hunan, China. [email protected].
  • 8 Guangzhou JYK Biotechnology Company Limited, Guangzhou, Guangdong, China. [email protected].
  • 9 Guangzhou Regenerative Medicine and Health Guangdong Laboratory, Guangzhou, Guangdong, China. [email protected].
  • 10 GZMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou, Guangdong, China. [email protected].
Abstract

Transient receptor potential ankyrin 1 (TRPA1), the non-selective cation channel, was found that can mediate the generation of multiple sclerosis, while the mechanism is still controversial. Lysophosphatidylcholine (LPC) is a critical trigger of multiple sclerosis which results from the syndrome of neuronal inflammation and demyelination. In this work, we suggested that TRPA1 can mediate the LPC-induced oxidative stress and cytotoxicity in OLN-93 oligodendrocyte. The expression of TRPA1 in OLN-93 was detected by using quantitative Real-Time PCR (qRT-PCR) and immunofluorescence. The calcium overload induced by LPC via TRPA1 was detected by calcium imaging. The mechanism of LPC-induced mitochondrial Reactive Oxygen Species (mtROS) generation, mitochondria membrane depolarization, nitric oxide (NO) increase, and development of superoxide production via TRPA1 was verified by using confocal imaging. The cell injury elicited by LPC via TRPA1 was confirmed by both CCK-8 and LDH cytotoxicity detection. These results indicate that TRPA1 plays an important role of the LPC-induced oxidative stress and cell damage in OLN-93 oligodendrocyte. Therefore, inhibition of TRPA1 may protect the LPC-induced demyelination.

Keywords

LPC; NO; Oligodendrocyte; ROS; TRPA1.

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