MicroRNA-122-5p alleviates endometrial fibrosis via inhibiting the TGF-ß/SMAD pathway in Asherman's syndrome.
Reprod Biomed Online
; 47(5): 103253, 2023 11.
Article
em En
| MEDLINE
| ID: mdl-37677924
ABSTRACT
RESEARCH QUESTION What is the effect of miR-122 on the progression and recovery of fibrosis in Asherman's syndrome? DESIGN:
Endometrial tissue was collected from 21 patients, 11 with intrauterine adhesion (IUA) and 10 without IUA. Quantitative real-time polymerase chain reaction, immunofluorescence and Western blot were applied to observe the expression of mRNAs/miRNAs and protein, respectively. The endometrial physical injury was carried out in C57BL/6 mice to create an endometrial fibrosis model, with intrauterine injection of adenovirus to compare the antifibrosis and repair function of miR-122 on endometrium. The morphology of the uterus was observed using haematoxylin and eosin staining, and fibrosis markers were detected by immunohistochemistry.RESULTS:
miR-122 expression was reduced in patients with IUAs, accompanied by fibrosis. MiR-122 overexpression reduced the degree of fibrosis in endometrial stromal cells. Further molecular analyses demonstrated that miR-122 inhibited fibrosis through the TGF-ß/SMAD pathway by directly targeting the 3' untranslated region of SMAD family member 3, suppressing its expression. Notably, miR-122 promoted endometrial regeneration and recovery of pregnancy capacity in a mouse endometrial injury model.CONCLUSIONS:
miR-122 is a critical regulator for repair of endometrial fibrosis and provided new insight for the clinical treatment of intrauterine adhesions.Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Doenças Uterinas
/
MicroRNAs
/
Ginatresia
Tipo de estudo:
Prognostic_studies
Limite:
Animals
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Female
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Humans
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Pregnancy
Idioma:
En
Revista:
Reprod Biomed Online
Ano de publicação:
2023
Tipo de documento:
Article