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Articles in PresS, published online ahead of print August 29, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00077.2002
Submitted on January 29, 2002
Accepted on August 20, 2002
1 Department of Medicine, Krannert Institute of Cardiology and Indiana Center for Vascular Biology and Medicine, Indianapolis, IN, USA; Department of Cardiology and Angiology, University of Munster, Muenster, NRW, Germany; Institute for Arteriosclerosis Research, University of Muenster, Muenster, NRW, Germany
2 Department of Molecular Genetics, Wyeth Genetics Institute, Andover, MA, USA
3 Department of Medicine, Krannert Institute of Cardiology and Indiana Center for Vascular Biology and Medicine, Indianapolis, IN, USA
4 Department of Cardiology and Angiology, University of Munster, Muenster, NRW, Germany; Institute for Arteriosclerosis Research, University of Muenster, Muenster, NRW, Germany
* To whom correspondence should be addressed. E-mail: sinderm{at}uni-muenster.de.
To study the effects of enhanced smooth muscle cell (SMC) proliferation on arterial vessel geometry in the absence of vessel trauma, we developed a transgenic mouse model expressing SV40 large T antigen under control of the 2.3 kb smooth muscle-myosin heavy chain promoter. Transgenic mice studied at ages from 3-13 weeks showed a 3.2-fold increase in arterial wall SMC-density, with 28% of SMC exhibiting proliferative cell nuclear antigen staining, confirming enhanced SMC proliferation, which was accompanied by 2-3-fold increases in arterial wall areas (p<0.05). Remarkably, despite increased vessel wall mass, the lumen area was not compromised, but rather was increased. A tightly conserved linear relationship was found between arterial circumference and wall thickness with slopes of 0.036 for both, transgenics (r=0.93, p<0.01) and controls (r=0.77, p<0.01), suggesting the hypothesis that the conservation of wall stress functions as a primary determinant of adaptive arterial remodeling. This establishes a new model of adaptive vessel remodeling occurring in response to a proliferative input, in the absence of mechanical injury or primary flow perturbation.
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