© 1999 American Heart Association, Inc.
Rapid Communications |
Cultured Porcine Coronary Artery Smooth Muscle Cells
A New Model With Advanced Differentiation
From the Department of Pathology (T.C., M.-L.B.-P., P.N., M.R., G.G.), University of Geneva-CMU, Geneva, Switzerland; Department of Molecular Cell Biology and Genetics (S.R., G.E.), University of Limburg, Maastricht, the Netherlands. The current affiliation for P.N. is Transgène S.A., Strasbourg, France.
Correspondence and reprints to Prof Giulio Gabbiani, University of Geneva-CMU, Department of Pathology, 1 rue Michel-Servet, 1211 Geneva 4, Switzerland. E-mail giulio.gabbiani{at}medecine.unige.ch
Abstract—Arterial
intimal thickening after endothelial injury induced in
rodents has proven to be a relatively unreliable model of
restenosis for testing clinically useful compounds. The same
has been found for cultured rat or rabbit vascular smooth muscle cells
(SMCs). To test alternative possibilities, we have studied several
differentiation features of porcine coronary artery SMCs,
cultured up to the 5th passage after enzymatic digestion of the media.
The effects of heparin, transforming growth factor
(TGF)-ß1 or TGF-ß2, and
all-trans-retinoic acid (tRA) on proliferation,
migration, and differentiation of these cells also were examined.
Porcine arterial SMCs in culture not only express high
levels of 
-smooth muscle (SM) actin but, contrary to rodent SMCs,
also maintain an appreciable expression of SM myosin heavy chain
isoforms 1 and 2, desmin, and smoothelin, a recently described late
differentiation marker of vascular SMCs. We demonstrate for the first
time that smoothelin is colocalized with -SM actin in these cells.
Finally, we show that in the porcine model, heparin is more potent than
TGF-ß1 or TGF-ß2 and tRA in terms of
inhibition of proliferation and migration and of increasing the
expression of differentiation markers. This model should be a useful
complement to in vivo studies of SMC differentiation and of
pathological situations such as restenosis and
atheromatosis.
Key Words: atheromatosis • restenosis • actin • smoothelin • myosin
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