The following is a summary of “MicroRNA-122-5p alleviates endometrial fibrosis via inhibiting the TGF-β/SMAD pathway in Asherman’s syndrome,” published in the November 2023 issue of Obstetrics and Gynecology by Chen, et al.
For a study, researchers sought to determine to what extent microRNA-122 influences the development of fibrosis and the healing process in patients with Asherman syndrome. The endometrial tissue of 21 individuals was obtained, 11 of them had intrauterine adhesion (IUA), while the other 10 patients did not have IUA. To observe the expression of mRNAs/miRNAs and protein, quantitative real-time polymerase chain reaction, immunofluorescence, and Western blot were used.
The endometrial physical damage was performed to generate a model of endometrial fibrosis. Additionally, an intrauterine injection of adenovirus was performed to evaluate the antifibrosis and healing function of miR-122 on the endometrium. Both hematoxylin and eosin staining and immunohistochemistry were used to study the morphology of the uterus. Additionally, fibrosis indicators were identified via investigation. There was a decrease in the expression miR-122 in patients who had IUAs, which was associated with fibrosis.
When endometrial stromal cells were overexpressed with miR-122, their degree of fibrosis decreased. The results of further molecular investigations revealed that miR-122 has the ability to reduce fibrosis by targeting the 3′ untranslated region of SMAD family member 3, therefore decreasing its expression. This inhibition was achieved via the TGF-β/SMAD pathway system. It is important to note that miR-122 contributed to the regeneration of endometrial tissue and the restoration of pregnancy potential in a model of endometrial damage. In addition to providing new insights for the therapeutic management of intrauterine adhesions, microRNA-122 is an essential regulator for the healing of endometrial fibrosis.
Source: sciencedirect.com/science/article/abs/pii/S1472648323003541
