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  • Title: miR-602 Activates NRF2 Antioxidant Pathways to Protect HBMECs from OGD/R-Induced Oxidative Stress via Targeting KEAP1 and HRD1.
    Author: Ma C, Yang L, Gao Q, Wang L.
    Journal: Dis Markers; 2022; 2022():6967573. PubMed ID: 36193504.
    Abstract:
    Blood brain barrier (BBB) dysfunction is a critical complication of diabetes mellitus type 2 (T2DM), and the oxidative stress-induced apoptosis of human brain microvascular endothelial cells (HBMECs) is a main cause of BBB dysfunction. In this study, oxygen and glucose deprivation/reoxygenation (OGD/R) models were established with HBMECs to analyze the effects of miR-602 on the apoptosis of HMBECs. Western Blot, qRT-PCR, CCK-8, flow cytometry assay, ROS detection assay, and dual-luciferase reporter gene assay were used to measure the expression levels of corresponding factors and changes in intracellular environment. The results showed that miR-602 was overexpressed in HBMECs after OGD/R treatment, and miR-602 could reduce ROS level of OGD/R-induced HBMECs and promote cells survival via increasing the expression level of NRF2 and the transcription activity of NRF2/ARE. Besides, it was found that KEAP1 and HRD1 were downstream factors of miR-602, and the increase of both KEAP1 and HRD1 could reverse the effects of miR-602 on the OGD/R-induced HMBECs. Therefore, miR-602 may be a potential target for research and treatment of the oxidative stress injury induced by apoptosis in HMBECs.
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