The Study Of The Targeting Mechanism Between MiR-214 And CTGF/CCN2 In Fibrosis Of Endometriosis In Vitro

BACKGROUND: As we know,mi R-214 and CTGF involved in heptic fibrosis.It is suggested that endometriosis fibrosis and other forms fibrosis share a similar pathogenetic mechanism.Thereby,we hypothesize that mi R-214 directly targeting CTGF mediate the mechanisms of fibrogenesis in endometriosis.METHODS: Endometrial and endometriosis tissues from 8(4 with and 4 without endometriosis)women with regular menstrual cycles were analyzed.Use TGF-? to mimic an in vitro endometrial fibrosis model,then divided them into two groups(group 1: treat with pre-mi R-214,group 2:treat with pre-mi R-214 and its antagomir).After 24 hours,all cells gone through immunofluorescence and RT-PCR to assess the level of fibrosis-associated proteins containing CTGF,?-SMA,and Collangen I,simultaneously analyze the relationship between them and mi R-214 in endometriosis fibrosis.RESULTS: Compared with nomal endometrium,this endometriotic lesions were more collagen fibrosis contraction by fibrotic markers(CCN2,?-SMA and Collagen I)were evident higher in endometriosis tissues,the expression of mi R-214 were significantly lower and the level of CTGF were higher than normal endometrium by hybridization in situ and immunohistochemistry.In endometrial fibrosis cell model,fibrotic markers express high level.After treat with mi R-214 mimics,the production of CCN2 or Collagen I protein was reduced(p<0.001 vs non treatment),some cells co-transfected with mi R-214 antagomirs,the expression of CCN2 or Collagen I protein was increased(p<0.001 vs non treatment).CONCLUSIONS: This study confirmed that mi R-214 could directly target CTGF to inhibit the evolvement of fibrosis and affect established fibrosis in endometriosis.