RTN1-C mediates cerebral ischemia/reperfusion injury via modulating autophagy. (29th December 2020)

• Record Type: Journal Article
• Authors: Ling, Jun; Cai, Haijian; Lin, Muya; Qi, Shunli; Du, Jian; Chen, Lijian
• Is Part Of: Acta biochimica et biophysica Sinica. Volume 53:Number 2(2021)
• Page Start: 170
• Page End: 178
• Publication Date: 2020-12-29
• Subjects: cerebral ischemia/reperfusion -- autophagy -- RTN1-C -- rapamycin; Biochemistry -- Periodicals; Biophysics -- Periodicals; 572.05
• DOI: 10.1093/abbs/gmaa162
• Languages: English
• ISSNs: 1672-9145

Abstract

Abstract: It has been widely accepted that autophagic cell death exacerbates the progression of cerebral ischemia/reperfusion (I/R). Our previous study revealed that overexpression of reticulon protein 1-C (RTN1-C) is involved in cerebral I/R injury. However, the underlying mechanisms have not been studied intensively. This study was designed to evaluate the effect of RTN1-C on autophagy under cerebral I/R. Using an in vitro oxygen-glucose deprivation followed by reoxygenation and a transient middle cerebral artery occlusion model in rats, we found that the expression of RTN1-C protein was significantly upregulated. We also revealed that RTN1-C knockdown suppressed overactivated autophagy both in vivo and in vitro, as indicated by decreased expressions of autophagic proteins. The number of Beclin-1/propidium iodide-positive cells was significantly less in the LV-shRTN1-C group than in the LV-shNC group. In addition, rapamycin, an activator of autophagy, aggravated cerebral I/R injury. RTN1-C knockdown reduced brain infarct volume, improved neurological deficits, and attenuated cell vulnerability to cerebral I/R injury after rapamycin treatment. Taken together, our findings demonstrated that the modulation of autophagy from RTN1-C may play vital roles in cerebral I/R injury, providing a potential therapeutic treatment for ischemic brain injury.