Overexpression of Igf2-derived Mir483 inhibits Igf1 expression and leads to developmental growth restriction and metabolic dysfunction in mice.

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Autor(es): dc.creatorSandovici, Ionel-
Autor(es): dc.creatorFernandez Twinn, Denise Sylvia-
Autor(es): dc.creatorCampbell, Niamh-
Autor(es): dc.creatorCooper, Wendy Nicola-
Autor(es): dc.creatorSekita, Yoichi-
Autor(es): dc.creatorZvetkova, Ilona-
Autor(es): dc.creatorFerland-McCollough, David-
Autor(es): dc.creatorProsser, Haydn Mark-
Autor(es): dc.creatorOyama, Lila Missae-
Autor(es): dc.creatorPantaleão, Lucas Carminatti-
Autor(es): dc.creatorCimadomo, Danilo-
Autor(es): dc.creatorQueiroz, Karina Barbosa de-
Autor(es): dc.creatorCheuk, Cecilia S. K.-
Autor(es): dc.creatorSmith, Nicola M.-
Autor(es): dc.creatorKay, Richard Graham-
Autor(es): dc.creatorAntrobus, Robin-
Autor(es): dc.creatorHoelle, Katharina-
Autor(es): dc.creatorMa, Marcella K. L.-
Autor(es): dc.creatorSmith, Noel H.-
Autor(es): dc.creatorGeyer, Stefan H.-
Autor(es): dc.creatorReissig, Lukas F.-
Autor(es): dc.creatorWeninger, Wolfgang Johann-
Autor(es): dc.creatorSiddle, Kenneth-
Autor(es): dc.creatorWillis, Anne E.-
Autor(es): dc.creatorLam, Brian Yee Hong-
Autor(es): dc.creatorBushell, Martin-
Autor(es): dc.creatorOzanne, Susan E.-
Autor(es): dc.creatorConstância, Miguel-
Data de aceite: dc.date.accessioned2025-08-21T15:36:12Z-
Data de disponibilização: dc.date.available2025-08-21T15:36:12Z-
Data de envio: dc.date.issued2025-02-11-
Data de envio: dc.date.issued2023-
Fonte completa do material: dc.identifierhttps://www.repositorio.ufop.br/handle/123456789/19739-
Fonte completa do material: dc.identifierhttps://doi.org/10.1016/j.celrep.2024.114750-
Fonte: dc.identifier.urihttp://educapes.capes.gov.br/handle/capes/1019483-
Descrição: dc.descriptionMir483 is a conserved and highly expressed microRNA in placental mammals, embedded within the Igf2 gene. Its expression is dysregulated in a number of human diseases, including metabolic disorders and certain cancers. Here, we investigate the developmental regulation and function of Mir483 in vivo. We find that Mir483 expression is dependent on Igf2 transcription and the regulation of the Igf2/H19 imprinting control region. Transgenic Mir483 overexpression in utero causes fetal, but not placental, growth restriction through insulin-like growth factor 1 (IGF1) and IGF2 and also causes cardiovascular defects leading to fetal death. Overexpression of Mir483 post-natally results in growth stunting through IGF1 repression, increased hepatic lipid production, and excessive adiposity. IGF1 infusion rescues the post-natal growth restriction. Our findings provide insights into the function of Mir483 as a growth suppressor and metabolic regulator and suggest that it evolved within the INS-IGF2-H19 transcriptional region to limit excessive tissue growth through repression of IGF signaling.-
Formato: dc.formatapplication/pdf-
Idioma: dc.languageen-
Direitos: dc.rightsaberto-
Direitos: dc.rightsThis is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/). Fonte: PDF do artigo.-
Palavras-chave: dc.subjectGenomic imprinting-
Palavras-chave: dc.subjectInsulin-like growth factor 2-
Título: dc.titleOverexpression of Igf2-derived Mir483 inhibits Igf1 expression and leads to developmental growth restriction and metabolic dysfunction in mice.-
Aparece nas coleções:Repositório Institucional - UFOP

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