ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2017
Dicer-dependent production of microRNA221 in hepatocytes inhibits p27 and is required for liver regeneration in mice.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- MicroRNA-183 accelerates the proliferation of hepatocyte during liver regeneration through targeting programmed cell death protein 6.Genes & genomics · 2022Article
- The Dynamic Interplay Between Mast Cells, Aging/Cellular Senescence, and Liver Disease.Gene expression · 2020Review
- Liver Regeneration in the Acute Liver Failure Patient.Clinics in liver disease · 2018Review
- Propofol induces apoptosis of breast cancer cells by downregulation of miR-24 signal pathway.Cancer biomarkers : section A of Disease markers · 2018Article
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6 authors.
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Abstract
Dicer processes microRNAs (miRs) into active forms in a wide variety of tissues, including the liver. To determine the role of Dicer in liver regeneration, we performed a series of in vivo and in vitro studies in a murine 2/3 hepatectomy model. Dicer was downregulated after 2/3 hepatectomy, and loss of Dicer inhibited liver regeneration associated with decreased cyclin A2 and miR-221, as well as increased levels of the cell cycle inhibitor p27. In vitro, miR-221 inhibited p27 production in primary hepatocytes and increased hepatocyte proliferation. Specific reconstitution of miR-221 in hepatocyte-specific Dicer-null mice inhibited p27 and restored liver regeneration. In wild type mice, targeted inhibition of miR-221 using a cholesterol-conjugated miR-221 inhibited hepatocyte proliferation after 2/3 hepatectomy. These results identify Dicer production of miR-221 as an essential component of a miRNA-dependent mechanism for suppression of p27 that controls the rate of hepatocyte proliferation after partial hepatectomy.
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