|
|
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Molecular Pharmacology Group, Division of Biochemistry and Molecular Biology, Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow, Scotland, United Kingdom
In this issue, Tilley and Maurice (p. 596) show that differentiation of vascular smooth muscle cells to a proliferative phenotype is associated with a profound up-regulation of specific phosphodiesterase-4 (PDE4) isoforms because of increased histone acetylation. The increased PDE4 activity is seen as preventing cAMP from inhibiting the enhanced proliferation, migration, and production of extracellular matrix seen in activated VSMC. This Perspective examines the proposal that selective inhibition of PDE4D1/2 could find use in adjunctive pharmacotherapy after percutaneous coronary interventions and, in addition, discusses the recent genetic evidence that PDE4D7 may provide a therapeutic target in stroke.
Address correspondence to: Miles Houslay, Division of Biochemistry and Molecular Biology, IBLS, Wolfson Building, University of Glasgow, Glasgow G12 8QQ, Scotland, UK. E-mail: m.houslay{at}bio.gla.ac.uk
This article has been cited by other articles:
![]() |
M. D. Houslay, G. S. Baillie, and D. H. Maurice cAMP-Specific Phosphodiesterase-4 Enzymes in the Cardiovascular System: A Molecular Toolbox for Generating Compartmentalized cAMP Signaling Circ. Res., April 13, 2007; 100(7): 950 - 966. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. T. Bender and J. A. Beavo Cyclic Nucleotide Phosphodiesterases: Molecular Regulation to Clinical Use Pharmacol. Rev., September 1, 2006; 58(3): 488 - 520. [Abstract] [Full Text] [PDF] |
||||