支气管平滑肌细胞中MK2 和MK3 过表达对细胞因子分泌的调节作用

目的:研究支气管平滑肌细胞中丝裂原活化蛋白激酶2/3(MK2/3)的过表达对细胞因子分泌的调节作用。方法:将野生型MK2和MK3腺病毒转染至人支气管平滑肌细胞中,Western blot实验检测MK2和MK3蛋白表达水平,确定转染腺病毒的最佳感染系数,检测热休克蛋白HSP27的磷酸化水平以及MK2和MK3过表达对MAPK和核因子(NF)-κB信号通路的影响。ELISA检测支气管平滑肌细胞分泌细胞因子的情况。结果:野生型MK2和MK3腺病毒转染至支气管平滑肌细胞的最佳感染系数为40,在支气管平滑肌细胞内有活性。MK2通过p38MAPK信号通路促进IL-6的分泌,抑制正常T细胞表达及趋化因子配体5(CCL5)的分泌,MK3通过NF-κB信号通路抑制RANTES/CCL5的分泌。结论:本研究揭示了MK2和MK3在支气管平滑肌细胞中通过不同的信号通路调节细胞因子的分泌,通过靶向MKs可调节支气管气道炎症反应。

Regulation of cytokine secretion by overexpression of MK2 and MK3 in bronchial smooth muscle cells

Objective:To investigate the Regulation of cytokine secretion related with the overexpression of MAPK-activated protein kinase(MKs)MK2 and MK3 which activated by mitogen in bronchial smooth muscle cells.Methods:Wild-type MK2 and MK3 adenovirus were transfected into human bronchial smooth muscle cells,The protein expression level of MK2 and MK3 were detected by Western blot to determine the optimal infection coefficient of the transfected adenovirus,and the phosphorylation level of heat shock protein HSP27 and the impact on Nuclear factor(NF)-κB signaling pathway of the overexpression of MK2 and MK3.The secretion of cytokines by bronchial smooth muscle cells was detected by ELISA.Results:Wild-type MK2 and MK3 adenopathy the optimal infection coefficient of virus transfection into bronchial smooth muscle cells was 40,and there was activity in bronchial smooth muscle cells.MK2 promotes secretion of IL-6 by white blood cells through the p38MAPK signaling pathway,and inhibits normal T cell expression and secretion of CCL5.MK3 inhibited the secretion of RANTES/CCL5 via the NF-B signaling pathway.Conclusion:This study revealed that MK2 and MK3 regulate cytokine secretion via different signaling pathways in bronchial smooth muscle cells.Bronchial airway inflammation can be regulated by targeting MKs.