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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:2184.)
© 2000 American Heart Association, Inc.

Vascular Biology

Determination of Temporal Expression Patterns for Multiple Genes in the Rat Carotid Artery Injury Model

Julie T. N. Tai; Eric E. Brooks; Shoudan Liang; Roland Somogyi; Jose D. Rosete; Richard M. Lawn; Dov Shiffman

From CV Therapeutics (J.T.N.T., E.E.B., J.D.R., R.M.L., D.S.) and Incyte Pharmaceuticals (S.L., R.S.) Palo Alto, Calif.

Correspondence to Dr Dov Shiffman, CV Therapeutics, 3172 Porter Dr, Palo Alto, CA 94304. E-mail ds{at}cvt.com

Abstract—Vascular injury induces extensive alteration to the extracellular matrix (ECM). These changes contribute to lesion formation and promote cell migration and proliferation. To elucidate ECM response to arterial injury, we used real-time polymerase chain reaction monitoring to quantitate the expression levels of 81 genes involved in the synthesis and breakdown of ECM as well as receptors and signaling proteins that communicate and respond to ECM molecules. The temporal regulation of gene expression in the carotid was measured at 1, 3, 5, 7, 9, 14, and 28 days postinjury. Among the 68 genes that showed detectable expression by our method, 47 (69%) were significantly induced or repressed over time, confirming the extensive ECM gene response in this model. More ECM-related genes (31) were regulated at day 1 than at any other time point, and the number of regulated genes decreased over time. However, 14 of the genes were still induced or repressed at day 28, indicating that return to preinjury expression patterns did not occur and no new steady state was achieved over 28 days. In spite of the large number of changes in gene expression, only a small number of expression patterns was observed, suggesting that ECM-related genes could potentially be coregulated.

Key Words: restenosis • carotid artery injury • gene expression profiling • extracellular matrix • matrix metalloproteinases

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