LncRNA53106调控CXCL10影响胰岛β细胞凋亡

目的研究长链非编码RNA(lncRNA)53106在炎症因子刺激MIN6细胞凋亡模型中的调控机制。方法建立MIN6胰岛细胞株炎症因子10 ng/ml白细胞介素-1β、50 ng/ml肿瘤坏死因子-α、50 ng/ml干扰素-γ刺激凋亡模型,采用流式细胞仪测凋亡率,实时定量PCR检测lncRNA53106和趋化因子10(CXCL10)的表达水平;构建lncRNA53106抑制剂和CXCL10的siRNA,分别敲低lncRNA53106和CXCL10,再用炎症因子联合刺激,通过流式细胞仪、实时定量PCR和Western印迹检测lncRNA53106、CXCL10、凋亡相关因子在MIN6细胞凋亡中的作用。结果在炎症因子刺激MIN6细胞凋亡模型中,炎症因子组凋亡率明显增加且具有统计学意义(P<0.01);敲低lncRNA53106再用炎症因子联合刺激,敲低组的凋亡率比对照组凋亡率明显减少且差异有统计学意义(P<0.05),实时定量PCR和Western印迹检测敲低组CXCL10表达亦减少,凋亡相关因子Bax和Caspase3的mRNA表达减少;敲低CXCL10再用炎症因子联合刺激,敲低组的凋亡率比对照组凋亡率明显减少且具有统计学意义(P<0.05),lncRNA53106表达稍有上升但差异无显著性(P=0.61)。结论lncRNA53106可能通过上调CXCL10,进而促进凋亡因子的表达,促进胰岛β细胞的凋亡,从而可能引起1型糖尿病的发生。

LncRNA53106 regulates CXCL10 and affects the apoptosis of islet β cells

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/mlinterferon-γin MIN6 islet cell lines were established.The apoptosis rate was measured by flow cytometry andthe expression levels of lncRNA53106 and(C-X-C motif)ligand(CXCL)10 were detected by realtime quantitativePCR(qPCR).LncRNA53106 smart silencer andCXCL10 siRNA were constructed,and lncRNA53106and CXCL10 were knocked down respectively.