Tie2-Cre Transgenic Mice: A New Model for Endothelial Cell-Lineage Analysis in Vivo
Open accessAbstract
Endocardial cells are thought to contribute at least in part to the formation of the endocardial cushion mesenchyme. Here, we created Tie2-Cre transgenic mice, in which expression of Cre recombinase is driven by an endothelial-specific promoter/enhancer. To analyze the lineage of Cre expressing cells, we used CAG-CAT-Z transgenic mice, in which expression of lacZ is activated only after Cre-mediated recombination. We detected pan-endothelial expression of the Cre transgene in Tie2-Cre;CAG-CAT-Z double-transgenic mice. This expression pattern is almost identical to Tie2-lacZ transgenic mice. However, interestingly, we observed strong and uniform lacZ expression in mesenchymal cells of the atrioventricular canal of Tie2-Cre;CAG-CAT-Z double-transgenic mice. We also detected lacZ expression in the mesenchymal cells in part of the proximal cardiac outflow tract, but not in the mesenchymal cells of the distal outflow tract and branchial arch arteries. LacZ staining in Tie2-Cre;CAG-CAT-Z embryos is consistent with endocardial-mesenchymal transformation in the atrioventricular canal and outflow tract regions. Our observations are consistent with previously reported results from Cx43-lacZ, Wnt1-Cre;R26R, and Pax3-Cre;R26R transgenic mice, in which lacZ expression in the cardiac outflow tract identified contributions in part from the cardiac neural crest. Tie2-Cre transgenic mice are a new genetic tool for the analyses of endothelial cell-lineage and endothelial cell-specific gene tar…
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TCDD toxicity and ductus venosus closure require AHR activation in hepatocytes and endothelial cells, respectively.
“To this end, Ahrfx was crossed to hepatocyte-specific (CreAlb) or endothelial-specific (CreTek) Cre recombinase to demonstrate that TCDD toxicity and the closure of the DV require receptor activation in hepatocytes and endothelial cells, respectively (Kisanuki et al., 2001; Postic et al., 1999; Walisser et al., 2005).”
From Rodent Genetic Models of Ah Receptor Signaling (2021) · cites this paper as Kisanuki et al., 2001
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- Authors
- Kisanuki, Y. Y., Hammer, R. E., Miyazaki, J.-I., Williams, S. C., Richardson, J. A., & Yanagisawa, M.
- Affiliations
- Howard Hughes Medical Institute (US)
- The University of Osaka (JP)
- The University of Texas Southwestern Medical Center (US)
- Venue
- Developmental Biology
- Publisher
- Elsevier BV
- Published
- 2001-02
- Volume
- 230
- Issue
- 2
- Pages
- 230-242
- ISSN
- 0012-1606 (ISSN-L)
- OpenAlex
- W1993913999
- Cited by
- 1,241
- References
- 1
- Citations by year
- 2026: 32 · 2025: 43 · 2024: 56 · 2023: 48 · 2022: 66 · 2021: 59 · 2020: 71 · 2019: 66 · 2018: 76 · 2017: 68 · 2016: 70 · 2015: 70 · 2014: 81 · 2013: 69 · 2012: 68
- FWCI
- 6.18
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Developmental Biology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Zebrafish Biomedical Research Applications
- Keywords
- cardiac outflow tract, atrioventricular canal, cardiac neural crest, Cre-mediated recombination
- MeSH terms
- Animals, beta-Galactosidase, Endocardium, Endothelium, Vascular, Enhancer Elements, Genetic, Embryonic and Fetal Development, Heart, Mice, Transgenic, Promoter Regions, Genetic, Viral Proteins, Gene Expression Regulation, Developmental, Integrases, Reverse Transcriptase Polymerase Chain Reaction, Receptor Protein-Tyrosine Kinases, Models, Animal, Receptor, TIE-2, Mice
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