LncRNA53106 regulates CXCL10 and affects the apoptosis of islet β cells / 中华内分泌代谢杂志

ABSTRACT

Objective To investigate the regulatory mechanism of long non-coding RNA ( lncRNA) 53106 in the apoptosis model of MIN6 cells stimulated by cytokines. Methods The stimulation model of cytokines 10 ng/ml interleukin-1β, 50 ng/ml tumor necrosis factor-α, 50 ng/ml interferon-γin MIN6 islet cell lines were established. The apoptosis rate was measured by flow cytometry and the expression levels of lncRNA53106 and ( C-X-C motif) ligand (CXCL)10 were detected by realtime quantitative PCR (qPCR). LncRNA53106 smart silencer and CXCL10 siRNA were constructed, and lncRNA53106 and CXCL10 were knocked down respectively. Then inflammatory cytokines were combined to stimulate, and their roles in the apoptosis of min6 cells were detected by flow cytometry, qPCR, and Western blotting. Results In the apoptosis model of MIN6 cells stimulated by cytokines, the apoptosis rate of cytokines group was significantly increased and reached statistical significance. The apoptosis rate of the knocked down lncRNA53106 group was significantly lower than that of the control group ( P<0.05) . The expression of CXCL10 was also decreased in the knockdown group by qPCR and Western blotting, the expressions of the apoptosis-related factors Bax and Caspase3 mRNA were decreased. The apoptosis rate in the knocked down CXCL10 group was significantly lower than that in the control group (P<0.05), and the expression of lncRNA53106 was slightly increased, but the difference was not significant ( P=0.61) . Conclusion LncRNA53106 may promote the expression of apoptosis factor by upregulation of CXCL10, and promote the apoptosis ofβcells of the pancreas, which may lead to the occurrence of type 1 diabetes.