ArticleIn vitro cellular & developmental biology. Animal2019
ATRA induces the differentiation of hepatic progenitor cells by upregulating microRNA-200a.
Article in In vitro cellular & developmental biology. Animal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- The role and mechanisms of vitamin A in suppressing hepatic stellate cell activation.Apoptosis : an international journal on programmed cell death · 2026Article
- The role of non-coding RNA regulates stem cell programmed death in disease therapy.Non-coding RNA research · 2025Review
- Autophagy modulates physiologic and adaptive response in the liver.Liver research (Beijing, China) · 2023Review
- Article
- Revisiting the miR-200 Family: A Clan of Five Siblings with Essential Roles in Development and Disease.Biomolecules · 2022Review
- Molecular pathways of liver regeneration: A comprehensive review.World journal of hepatology · 2021Review
- Mitomycin C Inhibits Esophageal Fibrosis by Regulating Cell Apoptosis and Autophagy via lncRNA-ATB and miR-200b.Frontiers in molecular biosciences · 2021Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Hepatic progenitor cells (HPCs) are potential seed cells for hepatocyte transplantation treatment of liver diseases. ATRA can induce the differentiation and mature function of hepatic progenitor cells, but the mechanism is still poorly understood. Here, by using microRNA array to analyze the expression profiles of microRNA (miR), we found that miR-200 family molecules in HPCs were upregulated after ATRA treatment, especially miR-200a-3p, 200c-3p, and 141-3p. ATRA induction could downregulate the expression of hepatic stem markers Oct4 and AFP, and improve the expression of hepatic markers ALB, CK18, and TAT, and the activity of ALB-GLuc, as well as indocyanine green uptake and glycogen storage function of HPCs. These above effects of ATRA on HPC differentiation were almost inhibited by blocking of miR-200a-3p, but not miR-200c-3p and 141-3p using antagomir. Cell autophagy is associated with ATRA regulation in HPCs, compared with control group, the expression of LC3 and Beclin1 increased in ATRA-treated HPCs, and orange and red fluorescent spot, which represents autophagy flow, also enhanced after ATRA treatment. However, ATRA-induced cell autophagy level was inhibited in antagomir-200a-3p+ATRA-treated cells. Therefore, the present study indicates that antagomir-200a-3p is related to ATRA-induced hepatic differentiation of HPCs through regulating cell autophagy, supporting the possible use of ATRA as a key inducer in HPC-based therapy of liver diseases.
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