LNC000152 participates in aluminum-induced reactive astrocyte proliferation by promoting GFAP expression

Abstract

Abstract Aluminum is a metal element with significant neurotoxicity, and there is a substantial correlation between aluminum exposure and cognitive dysfunction. GFAP is widely used as a marker of reactive astrocyte proliferation in response to pathological injury of the central nervous system. Studies of various neurodegenerative diseases have confirmed that the expression changes of GFAP are associated with nerve injury. We investigated the role of LNC000152 in aluminum-induced reactive proliferation of astrocytes. By establishing two aluminum-exposed cell models of primary rat astrocytes and CTX-TNA2 cell lines, we examined the expression of LNC000152 and GFAP, detected cell proliferation with EdU and cell cycle changes with flow cytometry. The effect of aluminum to promote glial cell proliferation was verified; the expression levels of LNC000152 and GFAP increased with the concentration of aluminum exposure. Intervention of LNC000152 expression by siRNA technology revealed that LNC000152 affected glial cell responsive proliferation by influencing GFAP expression. These results suggest that LNC000152 plays a role in the reactive proliferation of astrocytes induced by aluminum.