Regulation of the long noncoding RNA XIST on the inflammatory polarization of microglia in cerebral infarction
- Min Zhang
- Jian-Kai Yang
- Jing Ma
Affiliations: Department of Neurosurgery, The Second Affiliated Hospital of Xingtai Medical College, Xingtai, Hebei 054000, P.R. China, Department of Neurosurgery, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, P.R. China, Meteorological Service and Applied Meteorology, Ren County Meteorological Bureau of Hebei Province, Xingtai, Hebei 055150, P.R. China
- Published online on: June 30, 2021 https://doi.org/10.3892/etm.2021.10356
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Proinflammatory polarization of microglia aggravates brain injury in cerebral infarction. The present study focused on the role of long non‑coding (lnc)RNA X‑inactive specific transcript (XIST) in the phenotype modulation of microglia. It was revealed that lncRNA XIST was significantly upregulated in both a mouse cerebral infarction model induced by middle cerebral artery occlusion (MCAO) and an activated microglial model induced by oxygen/glucose deprivation (OGD). The overexpression of XIST enhanced the expression and release of pro‑inflammatory mediators [such as tumor necrosis factor (TNF)‑α, IL‑6, and iNOS] in microglia. Culture supernatant from lncRNA XIST‑overexpressed microglial cells induced the apoptosis of primary neurons, while TNF‑α antibody counteracted this neurotoxic effect. LncRNA XIST served as a sponge for miR‑96‑5p, counteracting its inhibitory effect on IKKβ/NF‑κB signaling and TNF‑α production. Notably, TNF‑α was positively regulated by XIST and in turn enhanced XIST expression in microglia. The lncRNA XIST‑TNF‑α feedback promoted the proinflammatory polarization of microglia, thereby exacerbating cerebral neuron apoptosis.