Journal
DEVELOPMENTAL DYNAMICS
Volume 235, Issue 12, Pages 3413-3422Publisher
WILEY
DOI: 10.1002/dvdy.20982
Keywords
endothelium; VE-cadherin; Cadherin-5; Cre-recombinase; tamoxifen; transgenic mice; tumor angiogenesis
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Funding
- NCI NIH HHS [R01-CA107002-01A1] Funding Source: Medline
- NHLBI NIH HHS [HL69766, HL074455] Funding Source: Medline
- NICHD NIH HHS [K120HD00850] Funding Source: Medline
- NIGMS NIH HHS [GM07104] Funding Source: Medline
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To introduce temporal control in genetic experiments targeting the endothelium, we established a mouse line expressing tamoxifen-inducible Cre-recombinase (Cre-ERT2) under the regulation of the vascular endothelial cadherin promoter (VECad). Specificity and efficiency of Cre activity was documented by crossing VECad-Cre-ERT2 with the ROSA26R reporter mouse, in which a floxed-stop cassette has been placed upstream of the beta-galactosidase gene. We found that tamoxifen specifically induced widespread recombination in the endothelium of embryonic, neonatal, and adult tissues. Recombination was also documented in tumor-associated vascular beds and in postnatal angiogenesis assays. Furthermore, injection of tamoxifen in adult animals resulted in negligible excision (lower than 0.4%) in the hematopoietic lineage. The VECad-Cre-ERT2 Mouse is likely to be a valuable tool to study the function of genes involved in vascular development, homeostasis, and in complex processes involving neoangiogenesis, such as tumor growth.
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