MicroRNA-210-3p Regulates Endometriotic Lesion Development by Targeting <i>IGFBP3</i> in Baboons and Women with Endometriosis

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Arquivos
art_KAI_MicroRNA2103p_Regulates_Endometriotic_Lesion_Development_by_Targeting_iIGFBP3i_2023.PDF (2.41 MB)
Citações na Scopus
3
Tipo de produção
article
Data de publicação
2023
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
SPRINGER HEIDELBERG
Autores
KAI, Kentaro
JOSHI, Niraj R.
BURNS, Gregory W.
HRBEK, Samantha M.
VEGTER, Erin L.
OCHOA-BERNAL, Maria Ariadna
SONG, Yong
MOLDOVAN, Genna E.
SEMPERE, Lorenzo F.
MIYADAHIRA, Eduardo H.
Citação
REPRODUCTIVE SCIENCES, v.30, n.10, p.2932-2944, 2023
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
MicroRNAs (miRs) play an important role in the pathophysiology of endometriosis; however, the role of miR-210 in endometriosis remains unclear. This study explores the role of miR-210 and its targets, IGFBP3 and COL8A1, in ectopic lesion growth and development. Matched eutopic (EuE) and ectopic (EcE) endometrial samples were obtained for analysis from baboons and women with endometriosis. Immortalized human ectopic endometriotic epithelial cells (12Z cells) were utilized for functional assays. Endometriosis was experimentally induced in female baboons (n = 5). Human matched endometrial and endometriotic tissues were obtained from women (n = 9, 18-45 years old) with regular menstrual cycles. Quantitative reverse transcript polymerase chain reaction (RT-qPCR) analysis was performed for in vivo characterization of miR-210, IGFBP3, and COL8A1. In situ hybridization and immunohistochemical analysis were performed for cell-specific localization. Immortalized endometriotic epithelial cell lines (12Z) were utilized for in vitro functional assays. MiR-210 expression was decreased in EcE, while IGFBP3 and COL8A1 expression was increased in EcE. MiR-210 was expressed in the glandular epithelium of EuE but attenuated in those of EcE. IGFBP3 and COL8A1 were expressed in the glandular epithelium of EuE and were increased compared to EcE. MiR-210 overexpression in 12Z cells suppressed IGFBP3 expression and attenuated cell proliferation and migration. MiR-210 repression and subsequent unopposed IGFBP3 expression may contribute to endometriotic lesion development by increasing cell proliferation and migration.
Palavras-chave
Endometriosis, MicroRNA-210, IGFBP3, Cell proliferation, Glandular epithelium
URI
https://observatorio.fm.usp.br/handle/OPI/57476
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Coleções
Artigos e Materiais de Revistas Científicas - FM/MOG