ArticleCell reports2024
Overexpression of Igf2-derived Mir483 inhibits Igf1 expression and leads to developmental growth restriction and metabolic dysfunction in mice.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Article
- Age-Related Epigenetic Drift Shapes Coordinated microRNA Promoter Methylation and Expression in Prostate Cancer.Epigenomes · 2026Article
- H19 and IGF2 imprinting from embryogenesis to oncogenesis.Frontiers in cell and developmental biology · 2026Review
- Placental Igf1 overexpression sex-specifically impacts mouse placenta structure, altering offspring striatal development and behavior.Experimental neurology · 2025Article
- A microRNA CRISPR screen reveals microRNA-483-3p as an apoptotic regulator in prostate cancer cells.Cell death & disease · 2025Article
- Advances in the Regulation of Lipid Metabolism by Non-Coding RNAs.Animals : an open access journal from MDPI · 2025Review
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Authors and funding
28 authors.
Funding
Abstract
Mir483 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.
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Registered trials
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