Circular RNA cZNF292 silence alleviates OGD/R-induced injury through up-regulation of miR-22 in rat neural stem cells (NSCs)

Abstract

Background Hypoxic-ischaemic encephalopathy (HIE) is a prevailing severe brain damage disease in newborns, and caused by perinatal asphyxia cerebral ischaemia and reperfusion. Here, we investigated the role of cZNF292 in oxygen-glucose deprivation/reperfusion (OGD/R)-induced neural stem cells (NSCs) injury, and explored the underlying molecular mechanism.Methods Before NSCs were subjected to OGD/R treatment, NSCs were transfected with or without overexpressing cZNF292, si-cZNF292 or miR-22 inhibitor. Viability, apoptosis and potential molecular mechanism were examined. Cell viability and apoptotic rate were evaluated utilizing cell counting kit-8 (CCK-8) and flow cytometry. The cZNF292 and miR-22 expression was determined utilizing quantitative reverse transcription-PCR (qRT-PCR). Moreover, apoptosis and Wnt/β-catenin and PKC/ERK pathways-associated proteins were quantified applying western blot.Results OGD/R repressed viability and promoted apoptosis of NSCs. Also, cZNF292 expression was promoted by OGD/R treatment. Moreover, cZNF292 overexpression further caused OGD/R-stimulated damage. Inversely, silencing cZNF292 alleviated OGD/R-stimulated damage in NSCs. In addition, miR-22 expression was negatively regulated by cZNF292. It was confirmed that silencing cZNF292 attenuated OGD/R-induced NSCs injury and promoted the activation of Wnt/β-catenin and PKC/ERK pathways via the up-regulation of miR-22.Conclusions The cZNF292 silence alleviated OGD/R-induced injury through the up-regulation of miR-22 in NSCs, and which furnished the theoretical basis for further research on HIE progression.

Keywords

• Oxygen-glucose deprivation/reperfusion
• cZNF292
• miR-22
• Wnt/β-catenin and PKC/ERK pathways