LINC00665 knockdown protects against cerebral ischemia-reperfusion injury

LINC00665 has been reported to participate in several human diseases. However, the role of LINC00665 in cerebral ischemia-reperfusion (CI/R) is still unknown. This study is designed to investigate the role of LINC00665 in rats with CI/R injury. We established middle cerebral artery occlusion/reperfusion (MCAO/R) rats model in vivo. PC12 cells treated with oxygen-glucose deprivation/reperfusion (OGD/R) were used to establish in vitro I/R model. RT-qPCR assay was adopted to assess the mRNA expression of LINC00665 and miR-744-5p. MTT assay was used to determine cell viability. The protein expression of Bax and Bcl-2 were detected by Western blot assay. The relationship between LINC00665 and miR-744-5p was confirmed by dual luciferase reporter assay and RNA immunoprecipitation (RIP). In this study, we found that LINC00665 was sharply up regulated in MCAO/R rats and PC12 cells treated with I/R. Functionally, LINC00665 knockdown attenuated oxidative damage in PC12 cells treated with I/R. Moreover, LINC00665 knockdown promoted cell viability, while inhibited cell apoptosis in PC12 cells treated with I/R. In addition, miR-744-5p was confirmed to be a target of LINC00665. LINC00665 knockdown was validated to project CI/R injury by sponging miR-744-5p expression.

Automated summary

The study revealed that LINC00665 plays a role in cerebral ischemia-reperfusion (CI/R) injury, and can affect cell viability and apoptosis by regulating miR-744-5p.