Phenotype commitment in vascular smooth muscle cells derived from coronary atherosclerotic plaques: differential gene expression of endothelial nitric oxide synthase.

M. L. Rossi, N. Marziliano, P. A. Merlini, E. Bramucci, U. Canosi, P. Presbitero, E. Arbustini, P. M. Mannucci, D. Ardissino

Research output: Contribution to journalArticle

Abstract

Unstable angina and myocardial infarction are the clinical manifestations of the abrupt thrombotic occlusion of an epicardial coronary artery as a result of spontaneous atherosclerotic plaque rupture or fissuring, and the exposure of highly thrombogenic material to blood. It has been demonstrated that the proliferation of vascular smooth muscle cells (VSMCs) and impaired bioavailabilty of nitric oxide (NO) are among the most important mechanisms involved in the progression of atherosclerosis. It has also been suggested that a NO imbalance in coronary arteries may be involved in myocardial ischemia as a result of vasomotor dysfunction triggering plaque rupture and the thrombotic response. We used 5' nuclease assays (TaqMan PCRs) to study gene expression in coronary plaques collected by means of therapeutic directional coronary atherectomy from 15 patients with stable angina (SA) and 15 with acute coronary syndromes (ACS) without ST elevation. Total RNA was extracted from the 30 plaques and the cDNA was amplified in order to determine endothelial nitric oxide synthase (eNOS) gene expression. Analysis of the results showed that the expression of eNOS was significantly higher (p

Original languageEnglish
Pages (from-to)39-46
Number of pages8
JournalEuropean journal of histochemistry : EJH
Volume49
Issue number1
Publication statusPublished - Jan 2005

ASJC Scopus subject areas

  • Cell Biology
  • Anatomy
  • Animal Science and Zoology
  • Developmental Biology

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