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Am J Physiol Cell Physiol (July 5, 2006). doi:10.1152/ajpcell.00092.2006
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Submitted on February 25, 2006
Accepted on June 23, 2006

Lack of Endothelial Nitric Oxide Synthase Decreases Cardiomyocyte Proliferation and Delays Cardiac Maturation

Erin Lepic1, Dylan Burger1, Xiangru Lu2, Wei Song, and Qingping Feng3*

1 Physiology and Pharmacology, University of Western Ontario, London, Canada; Cardiology Research Laboratory, Lawson Health Research Institute, London, Canada
2 Cardiology Research Laboratory, Lawson Health Research Institute, London, Canada
3 Physiology and Pharmacology, University of Western Ontario, London, Canada; Cardiology Research Laboratory, Lawson Health Research Institute, London, Canada; Medicine, University of Western Ontario, London, Canada

* To whom correspondence should be addressed. E-mail: qfeng{at}uwo.ca.

We recently demonstrated that deficiency in endothelial nitric oxide (eNOS) results in congenital septal defects and postnatal heart failure. The aim of this study was to investigate the role of eNOS in cardiomyocyte proliferation and maturation during postnatal development. Cultured eNOS-/- cardiomyocytes displayed fewer cells and lower BrdU incorporation in vitro compared to wild-type (WT) cardiomyocytes (P<0.05). Treatment with NO donor diethylenetriamine NONOate (DETA-NO) increased BrdU incorporation and cell counts in eNOS-/- cardiomyocytes (P<0.05). Inhibition of NOS activity using NG-nitro-L-arginine methyl ester (L-NAME) decreased the level of BrdU incorporation and cell counts in WT cardiomyocytes (P<0.05). Vascular endothelial growth factor (VEGF) increased the level of BrdU incorporation in cultured WT cardiomyocytes in a dose and time-dependent manner (P<0.05). Conversely, VEGF did not alter BrdU incorporation in eNOS-/- cardiomyocytes (P=n.s.). Furthermore, deficiency in eNOS significantly decreasd BrdU labeling indices in neonatal hearts in vivo. While WT hearts displayed a rapid decrease in ANP expression in the first week of neonatal life, ANP expression in eNOS-/- hearts remain elevated. Our study demonstrated that NO production from eNOS is necessary for postnatal cardiomyocyte proliferation and maturation, suggesting that eNOS plays an important role during postnatal heart development.




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 Cardiovasc ResHome page
L. Hammoud, F. Xiang, X. Lu, F. Brunner, K. Leco, and Q. Feng
Endothelial nitric oxide synthase promotes neonatal cardiomyocyte proliferation by inhibiting tissue inhibitor of metalloproteinase-3 expression
Cardiovasc Res, July 15, 2007; 75(2): 359 - 368.
[Abstract] [Full Text] [PDF]


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