MAP4/Mps1信号通路介导miR-21对心肌成纤维化细胞的影响  

Effect of MAP4/Mps1 Signaling Pathway Mediates miR-21 on Myocardial Fibroblast Cells

作　　者：蒋志明[1] JIANG Zhi-ming(Department of Cardiology,the Fourth Hospital of Changsha,Changsha 410006,Hunan,China)

机构地区：[1]长沙市第四医院心血管内一科,湖南长沙410006

出　　处：《医学信息》2023年第9期74-77,共4页Journal of Medical Information

基　　金：湖南省卫生健康委科研基金(编号:20203010270)。

摘　　要：目的探讨微管相关蛋白4/人单级纺锤体1信号通路介导miR-21促进心肌纤维化的作用。方法体外培养心肌成纤维细胞(CFs)并随机分为对照组、TGF-β1组、NC-miR-21组和TGF-β1+si-miR-21组;采用Western Bolt检测MAP4、p-MAP4、Mps1、p-Mps1、Ⅲ型胶原(ColⅢ)、Ⅰ型胶原(ColⅠ)、α平滑肌肌动蛋白(α-SMA);以试剂盒检测心肌细胞超氧化物歧化酶(SOD)和丙二醛(MDA)含量;酶联免疫吸附法(ELISA)检测各组细胞离心后的血清肿瘤坏死因子α(TNF-α)、白细胞介素-6(IL-6)及转化生长因子-β1(TGF-β1)水平。结果TGF-β1组MDA、未折叠蛋白MAP4、p-MAP4、Mps1、p-Mps1、TNF-α、IL-6、TGF-β1、ColⅢ、ColⅠ及α-SMA胶原蛋白水平高于对照组,SOD水平低于对照组(P<0.05);TGF-β1+si-miR-21组MDA、未折叠蛋白MAP4、p-MAP4、Mps1、p-Mps1、TNF-α、IL-6、TGF-β1、ColⅢ、ColⅠ及α-SMA胶原蛋白水平低于NC-miR-21组,SOD水平高于NC-miR-21组(P<0.05)。结论低表达miR-21可抑制心肌成纤维细胞ColⅢ、ColⅠ、α-SMA、TGF-β1的生物合成,其机制可能与Mps1/MAP4信号通路的激活调控有关。Objective To investigate the role of microtubule-associated protein 4/human single spindle 1 signaling pathway in miR-21 promoting myocardial fibrosis.Methods Cardiac fibroblasts(CFs)were cultured in vitro and randomly divided into control group,TGF-β1 group,NC-miR-21 group and TGF-β1+si-miR-21 group.Western Bolt was used to detect MAP4,p-MAP4,Mps1,p-Mps1,collagen typeⅢ(ColⅢ),collagen typeⅠ(ColⅠ),α-smooth muscle actin(α-SMA);the contents of superoxide dismutase(SOD)and malondialdehyde(MDA)in cardiomyocytes were detected by kit.The levels of serum tumor necrosis factor-α(TNF-α),interleukin-6(IL-6)and transforming growth factor-β1(TGF-β1)were detected by enzyme-linked immunosorbent assay(ELISA).Results The levels of MDA,unfolded protein MAP4,p-MAP4,Mps1,p-Mps1,TNF-α,IL-6,TGF-β1,ColⅢ,ColⅠandα-SMA collagen in TGF-β1 group were higher than those in control group,and the level of SOD was lower than that in control group(P<0.05).The levels of MDA,unfolded protein MAP4,p-MAP4,Mps1,p-Mps1,TNF-α,IL-6,TGF-β1,ColⅢ,ColⅠandα-SMA collagen in TGF-β1+si-miR-21 group were lower than those in NC-miR-21 group,and the level of SOD was higher than that in NC-miR-21 group(P<0.05).Conclusion Down-regulation miR-21 can inhibit the biosynthesis of ColⅢ,ColⅠ,α-SMA and TGF-β1 in myocardial fibroblasts,and the mechanism may be related to the activation and regulation of Mps1/MAP4 signaling pathway.

关 键 词：心肌纤维化 MIR-21 MAP4 MPS1 Α-SMA ColⅢ ColⅠ 

分 类 号：R285.5[医药卫生—中药学]