{"title":"Loss of miR-424 and miR-503 promotes decidualization of human endometrial stromal cells by increasing SCARA5 expression.","authors":"Tetsu Yamaguchi, Masashi Takamura, Hideno Tochigi, Yumi Mizuno, Yosuke Mizuno, Tomomi Sato, Shunsuke Tamaru, Kazuya Kusama, Kazuhiro Tamura, Yoshimasa Kamei, Takeshi Kajihara","doi":"10.1007/s00795-025-00431-5","DOIUrl":null,"url":null,"abstract":"<p><p>This study aims to investigate the function of miR-424 and miR-503, identified as putative regulatory miRNAs of FOXO1, a key factor for decidualization. The expression of both miR-424 and miR-503 in human endometrial stromal cells (HESCs) were measured before and after decidualization. Then, HESCs were transfected with both miR-424 and miR-503 before decidualization. Quantitative reverse transcription PCR, actin staining analysis, migration assay, fluorescence immunostaining, and luciferase assay were performed. MiR-424 and miR-503 expression was decreased after decidualization. Overexpression of both miR-424 and miR-503 inhibited major decidual maker genes, including FOXO1, PRL, IGFBP1, WNT4, and SCARA5, and altered F-actin's subcellular distribution from the periphery to all over the cytoplasm, concomitantly increasing cell mobility. Moreover, immunohistochemical analysis revealed overexpression of both miRNAs resulted in FOXO1 protein accumulation in the cytoplasm. Knocking down FOXO1 decreased SCARA5 expression, revealing SCARA5 is a downstream target of FOXO1. In addition, a luciferase reporter assay confirmed that the 3'-untranslated region of FOXO1 mRNA is targeted by miR-424. These results suggest that both miRNAs may play an important role in endometrial decidualization by regulating transcriptional activity of FOXO1, which alters decidualization-related gene expression such as SCARA5.Abstract: Journal standard instruction requires an unstructured abstract; hence structured abstract changed to unstructured.Thank you for the correction. I approve this change.</p>","PeriodicalId":18338,"journal":{"name":"Medical Molecular Morphology","volume":" ","pages":""},"PeriodicalIF":1.2000,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Medical Molecular Morphology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s00795-025-00431-5","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"PATHOLOGY","Score":null,"Total":0}
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Abstract
This study aims to investigate the function of miR-424 and miR-503, identified as putative regulatory miRNAs of FOXO1, a key factor for decidualization. The expression of both miR-424 and miR-503 in human endometrial stromal cells (HESCs) were measured before and after decidualization. Then, HESCs were transfected with both miR-424 and miR-503 before decidualization. Quantitative reverse transcription PCR, actin staining analysis, migration assay, fluorescence immunostaining, and luciferase assay were performed. MiR-424 and miR-503 expression was decreased after decidualization. Overexpression of both miR-424 and miR-503 inhibited major decidual maker genes, including FOXO1, PRL, IGFBP1, WNT4, and SCARA5, and altered F-actin's subcellular distribution from the periphery to all over the cytoplasm, concomitantly increasing cell mobility. Moreover, immunohistochemical analysis revealed overexpression of both miRNAs resulted in FOXO1 protein accumulation in the cytoplasm. Knocking down FOXO1 decreased SCARA5 expression, revealing SCARA5 is a downstream target of FOXO1. In addition, a luciferase reporter assay confirmed that the 3'-untranslated region of FOXO1 mRNA is targeted by miR-424. These results suggest that both miRNAs may play an important role in endometrial decidualization by regulating transcriptional activity of FOXO1, which alters decidualization-related gene expression such as SCARA5.Abstract: Journal standard instruction requires an unstructured abstract; hence structured abstract changed to unstructured.Thank you for the correction. I approve this change.
期刊介绍：
Medical Molecular Morphology is an international forum for researchers in both basic and clinical medicine to present and discuss new research on the structural mechanisms and the processes of health and disease at the molecular level. The structures of molecules, organelles, cells, tissues, and organs determine their normal function. Disease is thus best understood in terms of structural changes in these different levels of biological organization, especially in molecules and molecular interactions as well as the cellular localization of chemical components. Medical Molecular Morphology welcomes articles on basic or clinical research in the fields of cell biology, molecular biology, and medical, veterinary, and dental sciences using techniques for structural research such as electron microscopy, confocal laser scanning microscopy, enzyme histochemistry, immunohistochemistry, radioautography, X-ray microanalysis, and in situ hybridization.
Manuscripts submitted for publication must contain a statement to the effect that all human studies have been reviewed by the appropriate ethics committee and have therefore been performed in accordance with the ethical standards laid down in an appropriate version of the 1964 Declaration of Helsinki. It should also be stated clearly in the text that all persons gave their informed consent prior to their inclusion in the study. Details that might disclose the identity of the subjects under study should be omitted.
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