Generation of a conditional allele for the mouse endothelial nitric oxide synthase gene.

Jiang R, Wang S, Takahashi K, Fujita H, Fruci CR, Breyer MD, Harris RC, Takahashi T
Genesis. 2012 50 (9): 685-92

PMID: 22467476 · PMCID: PMC3399989 · DOI:10.1002/dvg.22026

Mice with endothelial nitric oxide synthase (eNOS) deletions have defined the crucial role of eNOS in vascular development, homeostasis, and pathology. However, cell specific eNOS function has not been determined, although an important role of eNOS has been suggested in multiple cell types. Here, we have generated a floxed eNOS allele in which exons 9-12, encoding the sites essential to eNOS activity, are flanked with loxP sites. Mice homozygous for the floxed allele showed normal eNOS protein levels and no overt phenotype. Conversely, homozygous mice with Cre-deleted alleles displayed truncated eNOS protein, lack of vascular NO production, and exhibited similar phenotype to eNOS knockout mice, including hypertension, low heart rate, and focal renal scarring. These findings demonstrate that the floxed allele is normal and it can be converted to a non-functional eNOS allele through Cre recombination. This mouse will allow time- and cell-specific eNOS deletion.

Copyright © 2012 Wiley Periodicals, Inc.

MeSH Terms (25)

Alleles Animals Blood Pressure Embryonic Stem Cells Endothelium Exons Female Gene Deletion Gene Targeting Genetic Engineering Heart Rate Homozygote Hypertension Integrases Kidney Lung Male Mice Mice, Inbred C57BL Mice, Knockout Models, Animal Nitric Oxide Nitric Oxide Synthase Type III Phenotype Recombination, Genetic

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