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Am J Physiol Heart Circ Physiol 283: H2714-H2724, 2002. First published August 29, 2002; doi:10.1152/ajpheart.00077.2002
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Vol. 283, Issue 6, H2714-H2724, December 2002

Smooth muscle-specific expression of SV40 large TAg induces SMC proliferation causing adaptive arterial remodeling

Jürgen R. Sindermann1,2,3, Philip Babij4, Joseph C. Klink1, Christiane Köbbert2,3, Gabriele Plenz2,3, Jan Ebbing2,3, Li Fan1, and Keith L. March1

1 Krannert Institute of Cardiology and Indiana Center for Vascular Biology and Medicine, Indiana University Medical Center, Indianapolis, Indiana 46202; 2 Department of Cardiology and Angiology and 3 Institute for Arteriosclerosis Research, University of Münster, 48149 Münster, Germany; and 4 Wyeth Genetics Institute, Andover, Massachusetts 01810

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 to 13 wk 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 two- to threefold 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.

cell proliferation; vascular remodeling; myosin heavy chain


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