SOCS3经JAK/STAT信号通路调控气道黏蛋白高分泌

SOCS3 regulates mucus hypersecretion via JAK/STAT signal pathway

目的研究细胞因子信号转导抑制因子3(SOCS3)在炎症情况下经JAK/STAT通路调控气道黏液高分泌。方法培养人气道16HBE上皮细胞,设置空白对照组、白介素(IL)-6处理组、IL-6和microRNA(miR)-203处理组,Western blot法分析细胞中磷酸化JAK激酶(p-JAK1/2)、SOCS3、黏蛋白(MUC)5AC蛋白水平;Real-time法检测各组细胞中SOCS3、STAT3、MUC5AC mRNA表达量;ELISA法检测各组培养上清液中p-JAK1/2、SOCS3、MUC5AC蛋白含量。结果在IL-6刺激下,IL-6处理组的p-JAK1/2、SOCS3、MUC5AC蛋白量及SOCS3、STAT3 mRNA含量较空白对照组显著升高(P<0.05),IL-6和miR-203处理组的p-JAK1/2、MUC5AC蛋白量及STAT3 mRNA含量较IL-6处理组显著升高(P<0.05),但SOCS3 mRNA与IL-6处理组比较差异无统计学意义,SOCS3蛋白含量较IL-6处理组显著降低(P<0.05)。结论细胞在IL-6刺激后SOCS3呈现高表达,同时经JAK/STAT信号通路负反馈调控MUC5AC。

Objective To investigate the SOCS3 regulates mucus hypersecretion via JAK/STAT signal pathway in inflammatory cells. Methods Culture 16HBE cells and divide into three groups： control group, inter leukin（IL） - 6-exposed group; IL-6-exposed and microRNA-203-transfered group. The protein levels of JAK1/2, SOCS3 and MUCSAC were measured by Western blot. The mRNA expressions of SOCS3, STAT3 and MUCSAC were detected by Real-time PCR. The protein levels of p-JAK1/2, SOCS3 and MUCSAC were analyzed by ELISA. Results Compared with the control group, the mRNA expressions of SOCS3, STAT3, MUCSAC and the protein levels of p- JAK1/2, SOCS3, MUCSAC were both significantly increased in IL-6-exposed group（P 〈 0. 05）; in the IL-6-ex- posed and miR-203-transfered group, the protein levels of p-JAK1/2, MUCSAC and the mRNA expressions of STAT3 were both significantly increased （P 〈 0. 05 ） , but the mRNA expressions of SOCS3 was almost as much as that in IL-6-exposed group, the protein levels of SOCS3 was significantly decreased （P 〈 0. 05 ）. Conclusion SOCS3 over-express when ceils are stimulated by IL-6, and negative-feedback regulates MUCSAC secretion via JAK/STAT signal pathway.