Fig. 5. Rescuing role of lncRNA Gm2199 in hepatic damages.

a Expression downregulation of three lncRNAs, Gm2199, 4930447J18Rik, and humanlincRNA1141, in mice with liver damages induced by CCl₄. The lncRNAs under study were selected from the differentially expressed lncRNA in hepatic damage, which were bioinformatically predicted to be involved in the regulation of liver damage related signaling pathways. The transcript levels were determined by qRT-PCR. N = 5 for each group. b Alterations of the expression of Gm2199, 4930447J18Rik, and humanlincRNA1141 in a mouse hepatocyte line, AML12. Hepatic damage was induced by pretreating AML12 cells with 15 mmol/L CCl₄ for 12 h. Note that only Gm2199 was found significantly downregulated in hepatic damage in vitro. N = 3 for each group. c The verification of overexpression of Gm2199 in AML12 and NCTC1469 cells transfected with pEGFP-N1-Gm2199 plasmid. N = 3 for each group. d The rescuing effect of lncRNA Gm2199 on the proliferation capacity of AML12 and NCTC1469 cells treated with CCl₄, as measured by CCK-8 assay. N = 3 for each group. Note that the transfection of pEGFP-N1-Gm2199 for Gm2199 overexpression abrogated the CCl₄-inuced diminishment of proliferation rate of AML12 cells, whereas the negative control construct failed to elicit any significant changes. The experiment data were converted to relative values over the control group and were expressed as mean ± SEM. *P < 0.05, **P < 0.01, and ***P < 0.001 vs. control; ^#P < 0.05, ^##P < 0.01 and ^###P < 0.001 vs. CCl₄. The rescuing effect of Gm2199 on the proliferation capacity of AML12 (e) and NCTC1469 (f), as measured by Edu staining. The scale bars represent 20 μm