| Authors |
Jiang R, Wang S, Takahashi K, Fujita H, Fruci CR, Breyer MD, Harris RC,
Takahashi T
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| Submitted By |
Takamune Takahashi on 10/31/2012 |
| Status |
Published |
| Journal |
Genesis (New York, N.Y. : 2000) |
| Year |
2012 |
| Date Published |
9/1/2012 |
| Volume : Pages |
50 : 685 - 692 |
| PubMed Reference |
22467476 |
| Abstract |
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. genesis 50:685-692, 2012. © 2012 Wiley
Periodicals, Inc.
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