MicroRNA miR-27b-3p regulate microglial inflammation response and cell apoptosis by inhibiting A20 (TNF-α-induced protein 3)

Abstract

Inflammatory reaction exerts a pivotal role in secondary damage after cerebral hemorrhage and spinal cord injury. miRNAs can both promote and inhibit inflammatory actions among microglial cells. The objective of the present paper was to figure out whether miR-27b-3p produced regulatory effects during processes of microglial inflammation. Lipopolysaccharides (LPS) were used to prepare microglial activation models. Following miR-27b-3p overexpression and interference, the RNA and protein levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β were subjected to real-time fluorescent quantitative PCR (qPCR) and western blot assays, respectively. Cellular apoptosis was subjected to flow cytometry and miR-27b-3p target genes were visualized using a dual luciferase reporter system for verification. The levels of TNF-α, IL-6, and IL-1β mRNA in miR-27b-3p-overexpressed microglial cells were markedly increased compared to the control. Apoptosis of microglial cells was increased markedly in the overexpressed miR-27b-3p group compared to the negative control. Conversely, a different result was presented in the microglial transfected with miR-27b-3p inhibitors. The downregulation of A20, a miR-27b-3p target gene, mediated levels of TNF-α, IL-6, and IL-1β. Furthermore, A20 reduced microglial apoptosis. These data revealed that miR-27b-3p could mediate not only microglia activation but also neuroinflammation via downregulating A20 expression. Thus, miR-27b-3p is regarded as gene therapy in treating cerebral hemorrhage and spinal cord injury.

Identification of Stage-Specific Differentially Expressed Genes and Network Meta-Analysis Reveals Potential Molecular Signatures in Chronic Hepatitis E Virus Infection

“…Recent report has demonstrated that HCV infection is mediated by miR-27b through downregulation of LIPC (hepatic lipase C) [92]. It has been documented that miR-27b-3p regulates microglial in ammation response and cell apoptosis through inhibition of A20 (TNF-α-induced protein 3) [93]. MiR-29c acts as tumor suppressive miRNA in the growth and advancement of HBV-related HCC by targeting TNFAIP3 (tumor necrosis factor alpha-induced protein 3) [94].…”

MiR-4739 inhibits the malignant behavior of esophageal squamous cell carcinoma cells via the homeobox C10/vascular endothelial growth factor A/phosphatidylinositol 3-kinase/AKT pathway

“…Dual-luciferase reporter assay was performed as previously described [ 35 ]. Cells (293 T) were seeded in 24-well plates, grown to a density of 50%, and then transfected with HOXC10 wild-type 3′-untranslated region (UTR) and HOXC10 mutant dual-luciferase reporter plasmids.…”

Mesenchymal Stem Cells from Familial Alzheimer’s Patients Express MicroRNA Differently

“…miR-27B is also increased in plasma extracellular vesicles, monocytes derived from blood, and brain tissue of patients with Alzheimer's [84,96,100], and it is downregulated in plasma of AD patients [42]. This pro-inflammatory microRNA triggers the activation of microglia and enhances the production of TNFα, IL-6, and IL-1β, as well as apoptosis [101]. Moreover, silencing LINC01128 inhibits glioma cells' proliferation, migration, and invasion levels by targeting miR-27B-3p [102].…”