Long Non-coding RNA LincRNA-erythroid Prosurvival (EPS) Alleviates Cerebral Ischemia/reperfusion Injury by Maintaining High-temperature Requirement Protein A1 (Htra1) Stability Through Recruiting Heterogeneous Nuclear Ribonucleoprotein L (HNRNPL)

Overview

Journal Bioengineered

Date 2022 May 13

PMID 35549989

Authors

Haifeng Guo

Xia Guo

Shiting Jiang

Affiliations

Soon will be listed here.

Abstract

This study aimed at investigating the role and mechanism of lincRNA-EPS (erythroid prosurvival) in cerebral ischemia/reperfusion (CIR) injury. The results showed that the overexpression of lincRNA-EPS was able to reduce the levels of interleukin-6, tumor necrosis factor-alpha and interleukin-1β stimulated in the OGD-treated Neuro-2a (N-2a) cells. The levels of reactive oxygen species and malondialdehyde were enhanced while the superoxide dismutase levels were reduced by oxygen and glucose deprivation (OGD) treatment, in which the lincRNA-EPS overexpression could reverse this effect in the cells. LincRNA-EPS interacted with high-temperature requirement protein A1 (Htra1) and heterogeneous nuclear ribonucleoprotein L (HNRNPL), and their depletion inhibited the Htra1 mRNA stability in N-2a cells. HNRNPL knockdown blocked lincRNA-EPS overexpression-induced Htra1 expression in the cells. The depletion of Htra1 could rescue lincRNA-EPS overexpression-mediated N-2a cell injury, inflammation, and oxidative stress induced by OGD. Functionally, lincRNA-EPS alleviates CIR injury of the middle cerebral artery occlusion/reperfusion mice . In conclusion, lincRNA-EPS attenuates CIR injury by maintaining Htra1 stability through recruiting HNRNPL.

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