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

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 durin...

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Bibliographic Details
Published in:Bioengineered 2021-12, Vol.12 (2), p.9902-9913
Main Authors: Li, Liping, Qi, Chao, Liu, Yuanyuan, Shen, Youliang, Zhao, Xia, Qin, Han, Zhang, Yi, Yu, Tengbo
Format: Article
Language:English
Subjects:
Animals
Apoptosis
cerebral hemorrhage
Cytokines - metabolism
inflammation
Inflammation - metabolism
Male
Mice
microglia
Microglia - metabolism
MicroRNAs - metabolism
miR-27b-3p
Research Paper
spinal cord injury
Tumor Necrosis Factor alpha-Induced Protein 3 - metabolism
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Summary: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.
ISSN:2165-5979
2165-5987
DOI:10.1080/21655979.2021.1969195