miR-16-5p Promotes Inflammation and Apoptosis in Oxygen-Glucose Deprivation Microglia Model by Mediating GPR30 Expression
10.12259/j.issn.2095-610X.S20251003
- VernacularTitle:miR-16-5p通过介导GPR30表达促进OGD模型小胶质细胞的炎症反应和凋亡
- Author:
Zhiyong LI
1
;
Zhenggang CHEN
;
Jun PENG
;
Dazhong LIANG
Author Information
1. 海南医科大学第一附属医院医疗质量管理科,海南 海口 570102
- Keywords:
Ischemic stroke;
miR-16-5p;
GPR30;
Inflammatory response;
Apoptosis
- From:
Journal of Kunming Medical University
2025;46(10):23-31
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the molecular mechanism of miR-16-5p promoting apoptosis and inflammatory response by targeting GPR30 expression in an in vitro ischemic stroke microglia model(BV-2).Methods An ischemic stroke cell model was established by subjecting BV-2 cells to oxygen-glucose deprivation(OGD).qRT-PCR was utilized to assess the levels of miR-16-5p and GPR30 mRNA in OGD cells.A miR-16-5p inhibitor was transfected into OGD cells to silence miR-16-5p expression,and alterations in inflammatory response and apoptosis were measured using ELISA kits and Annexin V-FITC/PI staining.Starbase was employed to predict interactions,and dual-luciferase reporter gene assays were conducted to confirm that miR-16-5p targets the 3'-untranslated region(UTR)sequence of GPR30.Changes in cellular inflammatory response and apoptosis were evaluated by knocking down miR-16-5p and/or GPR30 in OGD cells.Results miR-16-5p expression was significantly elevated(P<0.01),while GPR30 expression was notably decreased(P<0.01)in OGD-induced cells.Knockdown of miR-16-5p reduced the expression levels of inflammatory factors and the cell apoptosis ratio(P<0.01).Inhibition of miR-16-5p expression led to an upregulation of GPR30 mRNA and protein levels(P<0.01).Simultaneous silencing of both miR-16-5p and GPR30 partially enhanced inflammatory factor expression levels and the cell apoptosis ratio compared to cells transfected solely with the miR-16-5p inhibitor(P<0.05).Conclusion In the microglia OGD model,miR-16-5p triggers inflammatory responses and enhances apoptosis by inhibiting GPR30 expression.
