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Research Article Free access | 10.1172/JCI119805

Calmodulin-stimulated cyclic nucleotide phosphodiesterase (PDE1C) is induced in human arterial smooth muscle cells of the synthetic, proliferative phenotype.

S D Rybalkin, K E Bornfeldt, W K Sonnenburg, I G Rybalkina, K S Kwak, K Hanson, E G Krebs, and J A Beavo

Department of Pharmacology, University of Washington, Seattle 98195, USA.

Find articles by Rybalkin, S. in: PubMed | Google Scholar

Department of Pharmacology, University of Washington, Seattle 98195, USA.

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Department of Pharmacology, University of Washington, Seattle 98195, USA.

Find articles by Sonnenburg, W. in: PubMed | Google Scholar

Department of Pharmacology, University of Washington, Seattle 98195, USA.

Find articles by Rybalkina, I. in: PubMed | Google Scholar

Department of Pharmacology, University of Washington, Seattle 98195, USA.

Find articles by Kwak, K. in: PubMed | Google Scholar

Department of Pharmacology, University of Washington, Seattle 98195, USA.

Find articles by Hanson, K. in: PubMed | Google Scholar

Department of Pharmacology, University of Washington, Seattle 98195, USA.

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Department of Pharmacology, University of Washington, Seattle 98195, USA.

Find articles by Beavo, J. in: PubMed | Google Scholar

Published November 15, 1997 - More info

Published in Volume 100, Issue 10 on November 15, 1997
J Clin Invest. 1997;100(10):2611–2621. https://doi.org/10.1172/JCI119805.
© 1997 The American Society for Clinical Investigation
Published November 15, 1997 - Version history
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Abstract

The diversity among cyclic nucleotide phosphodiesterases provides multiple mechanisms for regulation of cAMP and cGMP in the cardiovascular system. Here we report that a calmodulin-stimulated phosphodiesterase (PDE1C) is highly expressed in proliferating human arterial smooth muscle cells (SMCs) in primary culture, but not in the quiescent SMCs of intact human aorta. High levels of PDE1C were found in primary cultures of SMCs derived from explants of human newborn and adult aortas, and in SMCs cultured from severe atherosclerotic lesions. PDE1C was the major cAMP hydrolytic activity in these SMCs. PDE expression patterns in primary SMC cultures from monkey and rat aortas were different from those from human cells. In monkey, high expression of PDE1B was found, whereas PDE1C was not detected. In rat SMCs, PDE1A was the only detectable calmodulin-stimulated PDE. These findings suggest that many of the commonly used animal species may not provide good models for studying the roles of PDEs in proliferation of human SMCs. More importantly, the observation that PDE1C is induced only in proliferating SMCs suggests that it may be both an indicator of proliferation and a possible target for treatment of atherosclerosis or restenosis after angioplasty, conditions in which proliferation of arterial SMCs is negatively modulated by cyclic nucleotides.

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