宫腔粘连（IUA）是子宫内膜损伤后发生的纤维化病变，严重威胁女性生殖健康，是临床亟待解决难题。miR-29以其在纤维化疾病中的调节作用而备受关注。项目组前期发现：IUA子宫内膜中TGF-β、Smad2和Smad3高表达，与IUA分期正相关；miR-29与TGF-β、Smad2及Smad3表达均呈负相关，初步证实miR-29与TGF-β/Smad通路相关，并可能参与IUA的发生。本研究拟：1) miR-29 mimic和miR-29 inhibitor分别转染子宫内膜间质细胞，检测纤维化进程；渐进延长TGF-β刺激细胞时间，上调miR-29，检测其逆转纤维化；TGF-β 3'UTR-psiCHECK-2和miR-29 mimic共转染子宫内膜间质细胞，证实TGF-β是miR-29靶基因；2)调控IUA模型miR-29水平，探讨可能作用机制。为阐明IUA发病机制、探寻治疗新方向提供理论基础。

Intrauterine adhesions (IUA) as the terminations of aberrant fibrosis after endometrium injury，was a urgently clinical puzzle for seriously threatening to female reproductive health. miRNA was concerned about the important role in regulation of fibrosis pathway in multiple organ fibrosis disease. Earlier stage of project terms detected that: the high expression of TGF-β, Smad2 and Smad3 in IUA endometria positively correlating with the severity of the IUA; the level of miR-29 having a negative correlation with protein expression of TGF-β, Smad2 and Smad3 in IUA. This fact preliminary confirmed miR-29 might control and regulate the TGF-β/Smad signaling pathways and involve in the occurrence of IUA. On this basis ,the investigation design to: 1) Respectively construct plasmid with mimicker and inhibitor of miR-29, transfection endometrial stroma cells, test the fibrosis; gradually increasing TGF-β stimulation of endometrial stromal cells in time, up-regulation of miR-29 level, test its role in reversing the process of fibrosis, and to further clarify the signaling pathways in regulation of fibrosis; confirm that TGF-β is the target genes of miR-29 by being co-transfected TGF-β 3'UTR-psiCHECK-2 and miR-29 with endometrial stromal cells; 2) Regulate miR-29 level in vivo of IUA animal models, elucidate its role in the process of IUA fibrosis, provide a new theoretical foundation to clarify the pathogenesis of IUA, and provide new targets for the treatment.