Inhibitory activity of clinical thiazolidinedione peroxisome proliferator activating receptor-γ ligands toward internal mammary artery, radial artery, and saphenous vein smooth muscle cell proliferation

de Dios, Stephanie T., Bruemmer, Dennis, Dilley, Rodney J., Ivey, Melanie E., Jennings, Garry L.R., Law, Ronald E. and Little, Peter J. (2003) Inhibitory activity of clinical thiazolidinedione peroxisome proliferator activating receptor-γ ligands toward internal mammary artery, radial artery, and saphenous vein smooth muscle cell proliferation. Circulation, 107 20: 2548-2550. doi:10.1161/01.CIR.0000074040.31731.96


Author de Dios, Stephanie T.
Bruemmer, Dennis
Dilley, Rodney J.
Ivey, Melanie E.
Jennings, Garry L.R.
Law, Ronald E.
Little, Peter J.
Title Inhibitory activity of clinical thiazolidinedione peroxisome proliferator activating receptor-γ ligands toward internal mammary artery, radial artery, and saphenous vein smooth muscle cell proliferation
Journal name Circulation   Check publisher's open access policy
ISSN 0009-7322
1524-4539
Publication date 2003-05-27
Sub-type Article (original research)
DOI 10.1161/01.CIR.0000074040.31731.96
Open Access Status Not yet assessed
Volume 107
Issue 20
Start page 2548
End page 2550
Total pages 3
Place of publication Philadelphia, PA, United States
Publisher Lippincott Williams & Wilkins
Language eng
Formatted abstract
Background: The proliferation of vascular smooth muscle cells (VSMCs) is a known response to arterial injury that is an important part of the process of restenosis and atherosclerosis. People with diabetes have an increased risk of cardiovascular disease resulting from accelerated coronary atherosclerosis. The newest drugs for Type 2 diabetes are thiazolidinediones, which are insulin-sensitizing peroxisome proliferator activating receptor-γ (PPARγ) ligands. We investigated the antiproliferative effects of troglitazone, rosiglitazone, and pioglitazone on VSMCs derived from the three vascular beds used for coronary artery by-pass grafting: the internal mammary and radial artery and saphenous veins.

Methods and Results: The three vessels yielded proliferating cells of slightly differing morphology. Inhibition of cell proliferation was assessed by cell counting and cell cycle studies by Western blotting for phosphorylated retinoblastoma protein. All three thiazolidinediones showed inhibitory potency toward cell proliferation with a potency troglitazone>rosiglitazone≈pioglitazone, and this potency profile was maintained toward the growth factor and insulin-stimulated phosphorylation of the retinoblastoma protein, which controls cell cycle progression.

Conclusion: The inhibitory potency of clinical thiazolidinediones toward different vascular sources is dependent on the individual thiazolidinedione and very little on the vascular source.
Keyword Diabetes mellitus
Grafting
Muscle, smooth
Restenosis
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Pharmacy Publications
 
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