miR-30b protects microglia deprived with oxygen and glucose via regulating inflammatory response

Author(s): Jingbo Li, Shuda Chen, Jing Meng, Gao Zhang, Reng Ren*

AbstractIschemic stroke is considered to be the leading cause of mortality and morbidity through the world. In the present study, we evaluated the role of miR-30b and its direct target, mixed lineage kinase 4 (MLK4), in ischemic stroke in an in vitro model. Murine microglia BV-2 cells were cultured with oxygen-glucose deprivation (OGD). Expression changes of miR-30b and MLK4 were detected. BV-2 cells were then transfected with miR-30b mimic. The impact of miR-30b expression level on cellular apoptosis, expression of MLK4, and expression of inflammatory factors were measures. Dual-luciferase reporter assay was performed to test the direct targeting relation between miR-30b and MLK4. OGD treatment significantly down-regulated the level of miR-30b, while up-regulated both the protein and mRNA levels of MLK4 in a time-dependent manner. The expression of MLK4 was negatively regulated by miR-30b by a direct interaction. The addition of miR-30b mimic significantly inhibited the apoptosis induced by OGD treatment. Moreover, the increased levels of inflammatory cytokines, such as IL-1β, IL-6 and TNF-α, under OGD condition, were also decreased by miR-30b mimic. In conclusion, miR-30b protects microglia via inhibiting the apoptosis and inflammation under OGD condition. Therefore miR-30b might be a new therapeutic target for ischemic stroke.

 

Keywords: miR-30b, mixed lineage kinase 4, oxygen-glucose deprivation, inflammation, apoptosis, molecular pathology
Adv.Bio.Med.: 2018, Vol.3(No.2),pp:31-43
DOI: