Inhibition of GPR4 attenuates SH-SY5Y cell injury in cerebral ischemia/reperfusion via anti-apoptotic pathways

Chunli  Xing; Guizhen Yan; Qishuai  Liu

doi:10.18388/abp.2020_5497

Inhibition of GPR4 attenuates SH-SY5Y cell injury in cerebral ischemia/reperfusion via anti-apoptotic pathways

Chunli Xing Department of Neurology, People’s Hospital of Lixia District of Jinan, Jinan City, Shandong Province, 250014, China
Guizhen Yan Department of Neurology, People’s Hospital of Lixia District of Jinan, Jinan City, Shandong Province, 250014, China https://orcid.org/0000-0002-2797-0491
Qishuai Liu Department of Neurology, The First Hospital of Zibo, Zibo City, Shandong Province, 255200, China

DOI: https://doi.org/10.18388/abp.2020_5497

Abstract

Cerebral ischemia/reperfusion injury (CIRI) can lead to increased vascular endothelial permeability and blood-brain barrier damage in patients with stroke. G protein-coupled receptor 4 (GPR4) is a functional pH sensor that plays a key role in renal ischemia-reperfusion-induced apoptosis. However, whether GPR4 has a role in cerebral ischemia remains to be further studied. Our study found that after oxygen-glucose deprivation/reoxygenation (OGD/R) treatment, the levels of GPR4 and CHOP in SH-SY5Y cells were significantly increased, which was accompanied by a decrease in cell viability, and an increase in LDH release and apoptosis. After knockdown of GPR4 using shRNA, CHOP levels in SH-SY5Y cells were also decreased, which unexpectedly increased cell activity and decreased LDH release and apoptosis rate. Interestingly, CHOP overexpression reversed the effect of GPR4 knockdown, suggesting that OGD/R-induced CIRI may involve endoplasmic reticulum stress-related apoptosis. In conclusion, our study provided a basis for further research on the mechanism of CIRI.

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Published

2021-04-07

Issue

Vol. 68 No. 2 (2021)

Section

Articles

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