ArticleThe American journal of pathology2009
A mouse model of inducible liver injury caused by tet-on regulated urokinase for studies of hepatocyte transplantation.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 25 citations in OpenAlex.
- Single-nucleus RNA sequencing reveals HBV-driven metabolic reprogramming and TIMP1-mediated fibrosis in human-liver-chimeric mice.Frontiers in cellular and infection microbiology · 2025Article
- Discovering human cell-compatible gene therapy virus variants via optimized screening in mouse models.Cell proliferation · 2024Article
- [Research progress of mouse model of hepatitis B virus infection].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2023Article
- Inducible overexpression of a FAM3C/ILEI transgene has pleiotropic effects with shortened life span, liver fibrosis and anemia in mice.PloS one · 2023Article
- Generation of qualified clinical-grade functional hepatocytes from human embryonic stem cells in chemically defined conditions.Cell death & disease · 2019Article
- A two-step lineage reprogramming strategy to generate functionally competent human hepatocytes from fibroblasts.Cell research · 2019Article
- Generation of functional human hepatocytes in vitro: current status and future prospects.Inflammation and regeneration · 2019Review
- Transplantation of hESC-derived hepatocytes protects mice from liver injury.Stem cell research & therapy · 2015Article
- New horizons for studying human hepatotropic infections.The Journal of clinical investigation · 2010Article
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8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mouse models of liver injury provide useful tools for studying hepatocyte engraftment and proliferation. A representative model of liver injury is the albumin-urokinase (Alb-uPA) transgenic model, but neonatal lethality hampers its widespread application. To overcome this problem, we generated a transgenic mouse in which transcription of the reverse tetracycline transactivator was (rtTA) driven by the mouse albumin promoter, and backcrossed the rtTA mice onto severe combined immunodeficient (SCID)/bg mice to generate immunodeficient rtTA/SCID mice. We then produced recombinant adenoviruses Ad.TRE-uPA, in which the urokinase was located downstream of the tetracycline response element (TRE). The rtTA/SCID mouse hepatocytes were then infected with Ad.TRE-uPA to establish an inducible liver injury mouse model. In the presence of doxycycline, uPA was exclusively expressed in endogenous hepatocytes and caused extensive liver injury. Enhanced green fluorescent protein-labeled mouse hepatocytes selectively repopulated the rtTA/SCID mouse liver and replaced over 80% of the recipient liver mass after repeated administration of Ad.TRE-uPA. Compared with the original uPA mice, rtTA/SCID mice did not exhibit problems regarding breeding efficiency, and the time window for transplantation was flexible. In addition, we could control the extent of liver injury to facilitate transplantation surgery by regulating the dose of Ad.TRE-uPA. Our inducible mouse model will be convenient for studies of hepatocyte transplantation and hepatic regeneration, and this system will facilitate screening for potential genetic factors critical for engraftment and proliferation of hepatocytes in vivo.
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