Effects of lncRNA Tmevpg1 on the Expression of Mouse Autophagy and Key Signaling Molecules in JAK-STAT Signaling Pathways
Wang Xian, Wang Hongxia, Pan Junfei, Fang Yuan, Guo Le, Xu Guangxian*
This study was performed to explore the effect of lncRNA Tmevpg1 on the expression levels of mouse autophagy and key signaling molecules in JAK-STAT signaling pathway. In this study, Tmevpg1, JAKSTAT signaling pathway and autophagy interaction regulatory network were constructed by bioinformatics analysis; The mouse autophagy model was constructed with rapamycin (Rapa) and chloroquine (CQ), and the cell model of Tmevpg1 overexpression and interference was constructed by cell co-culture technique. The relative expression of Tmevpg1 and other related molecules were detected by qRT-PCR in mouse spleen issues and cell model, and Western blot verified the expression of autophagy-associated proteins, T-bet and phosphorylated proteins in key signaling molecules of JAK-STAT pathways. The results showed that Tmevpg1, IFN-γ, T-bet, STAT1 and JAK1 were significantly up-regulated at a certain time point of autophagy (P<0.001). After overexpression of Tmevpg1, ULK1 expression was up-regulated (P<0.05), p62 was down-regulated (P<0.05), IFN-γ, T-bet, JAK1 and STAT1 expression did not change significantly, but IFN-γ, T-bet, JAK1 and STAT1 expression were down-regulated after interference with Tmevpg1 (P<0.05). Western blot results showed that the autophagy model of mice was successfully constructed, and the expression trends of T-bet, p-STAT1 and p-JAK1 were consistent with the level of mRNA. Overexpression of Tmevpg1 can up-regulate ULK1 and LC3-II and down-regulate p62. At the same time, the expression of T-bet, p-JAK1 and p-STAT1 decreased after interference with Tmevpg1. In conclusion, our research suggest that lncRNA Tmevpg1 and the JAK-STAT signaling pathway may play critical regulatory roles in autophagy.
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