G-CSF通过MCTP1-AS1/SMAD7表观遗传调控途径抑制上皮间质化转变促进子宫内膜修复  

G-CSF inhibits epithelial-mesenchymal transformation and promotes endometrial repair through the MCTP1-AS1/SMAD7 epigenetic regulatory pathway

作　　者：贺泓霓 王江 胡辉权[1] 袁心柱 He Hongni;Wang Jiang;Hu Huiquan;Yuan Xinzhu(Department of Gynecology,the Affiliated Nanchong Central Hospital of North Sichuan Medical College,Nanchong Sichuan 637000,P.R.China;Department of Nephrology,the Affiliated Nanchong Central Hospital of North Sichuan Medical College,Nanchong Sichuan 637000,P.R.China)

机构地区：[1]川北医学院附属南充市中心医院妇科,四川南充637000 [2]川北医学院附属南充市中心医院肾脏内科,四川南充637000

出　　处：《中国计划生育和妇产科》2023年第8期42-45,共4页Chinese Journal of Family Planning & Gynecotokology

基　　金：南充市科技计划项目(项目编号:22JCYJPT0011)。

摘　　要：目的探究粒细胞集落刺激因子(granulocyte colony-stimulating factor,G-CSF)通过多个C2结构域和跨膜区蛋白1反义RNA1(MCTP1 antisense RNA 1,MCTP1-AS1)/SMAD家族成员7(SMAD family member 7,SMAD7)表观遗传调控途径抑制上皮间质化转变(epithelial-mesenchymal transition,EMT)促进子宫内膜修复,并探讨其可能的潜在作用机理。方法通过qRT-PCR检测人宫颈内膜细胞H8细胞中G-CSF、E-钙黏蛋白(E-cadherin)、紧密连接蛋白Z0-1、N-钙黏蛋白(N-cadherin)、波形蛋白(Vimentin)、SMAD7以及MCTP1-AS1的表达水平。MCTP1-AS1与G-CSF的相互作用采用双荧光素酶报告基因实验验证。结果G-CSF过表达可能抑制N-cadherin和Vimentin的表达,促进E-cadherin和Z0-1的表达(P<0.05);而在沉默G-CSF后可能促进了N-cadherin和Vimentin的表达,抑制E-cadherin和Z0-1的表达(P<0.05)。G-CSF靶向MCTP1-AS1。过表达的G-CSF可以抑制MCTP1-AS1和SMAD7的表达;相反,当G-CSF被敲除时,MCTP1-AS1和SMAD7的表达水平明显上调。结论通过细胞实验证实了G-CSF可能通过MCTP1-AS1/SMAD7表观遗传调控途径抑制上皮间质化转变促进子宫内膜修复,同时表明G-CSF可能是用于治疗薄型子宫的一个新靶点。Objective To explore the effect of granulocyte colony-stimulating factor(G-CSF)through multiple C2 domains and transmembrane protein 1 antisense RNA1(MCTP1 antisense RNA1,MCTP1-AS1)/SMAD family member 7(SMAD7)epigenetic regulation pathway inhibited epithelial-mesenchymal transition(EMT)and promoted endometrial repair and its potential mechanism.Methods The expression levels of G-CSF,E-cadherin,tight junction protein Z0-1,N-cadherin,Vimentin,SMAD7 and MCTP1-AS1 in H8 cells of human endocervical cells were determined by qRT-PCR.The interaction between MCTP1-AS1 and G-CSF was verified by double luciferase reporter gene assay.Results Overexpression of G-CSF possibly inhibited the expression of N-cadherin and Vimentin,and promoted the expression of E-cadherin and Z0-1(P<0.05);after silencing G-CSF,the expression of N-cadherin and Vimentin was possibly promoted,and the expression of E-cadherin and Z0-1 was inhibited(P<0.05).G-CSF targeted MCTP1-AS1.Overexpressed G-CSF inhibited the expression of MCTP1-AS1 and SMAD7;in contrast,when G-CSF was knocked out,the expression levels of MCTP1-AS1 and SMAD7 were significantly up-regulated.Conclusion Cell experiments confirmed that G-CSF inhibited epithelial-mesenchymal transformation and promoted endometrial repairing through MCTP1-AS1/SMAD7 epigenetic regulation pathway,and indicated that G-CSF may be a new target for the treatment of thin uterus.

关 键 词：G-CSF 上皮-间质转化 MCTP1-AS1 SMAD7 子宫内膜修复 

分 类 号：R711.74[医药卫生—妇产科学]