Fat mass- and obesity-associated gene promotes ectopic endometriotic stromal cells fibrosis via TLR2/p38 axis
WANG Han1, DUAN Ping2
1.Department of Gynecology, the Second Hospital of Harbin Medical University, Harbin 150000, China; 2.Department of Gynecology, the Second Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China
WANG Han,DUAN Ping. Fat mass- and obesity-associated gene promotes ectopic endometriotic stromal cells fibrosis via TLR2/p38 axis[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2022, 52(3): 180-185,193.
Abstract：Objective: To investigate the effect of FTO on fibrosis of ectopic endometrial mesenchymal cells (eESCs). Methods: m6A-related genes in endometriosis (EMs) were screened and detected, using quantitative real-time polymerase chain reaction (qRT-PCR). Detection of fibrosis-related gene expression in eESCs by overexpression of FTO in a lentiviral vector. Relationship between FTO and TLR2 in eESCs predicted and validated by m6A2 Target site and MeRIP-qPCR. Protein changes in p38 were detected by Western blot. Results:FTO expression was down-regulated in EMs (P<0.05). FTO overexpression promoted fibrosis and inhibited proliferation of eESCs (P<0.05). FTO upregulated its protein level through m6A modification of TLR2 in eESCs (P<0.05). FTO promoted cell fibrosis through TLR2/p38 signaling pathway in eESCs (P<0.05). Conclusion:FTO is low expressed in EMs and upregulation of FTO promotes fibrosis of eESCs through TLR2/p38 signaling pathway.
