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P63 Introduction: The molecular events in  atherosclerotic carotid disease that trigger responses within the  plaque resulting in plaque instability and thromboembolic  cerebrovascular sequelae are unclear. Plaque instability may be related  to apoptosis and extracellular matrix degradation. We compared  atheromatous and fibrous plaques in terms of apoptosis,  apoptosis-related proteins, cell cycle regulatory genes, death  substrates for apoptosis, proteolytic activity and infiltrating cells.Methods: Apoptosis was detected in carotid endarterectomy  plaques by the TUNEL assay. Immunohistochemical studies were performed  to identify macrophages and infiltrating cells, localize the expression  of bcl-2, bax, cyclin D-1, caspases, Fas, PARP, MMP-2 and MMP-9.  Zymography was used to compare the proteolytic activity levels in the  two types of plaques.Results: There were no inflammatory  cells in the fibrous plaques. Apoptotic cell death was significantly  higher (p&lt;0.001) in atheromatous plaques as compared to fibrous  plaques. Elevated levels of proteinases in atheromatous plaques were  noted. There were significant increases in the expression of  pro-apoptotic protein, bax (p&lt;0.01), Fas (p&lt;0.04), and CPP-32  (p&lt;0.001) in atheromatous plaques as compared to fibrous plaques.  Localization of bcl-2 in atheromatous as well as fibrous plaques was  similar. There was differential expression of cell cycle protein,  cyclin D-1.Conclusions: The greater amount of apoptosis and  overexpression of mediators of apoptosis seen in atheromatous plaques  suggest that deregulated apoptosis may be involved in the pathogenesis  of unstable atherosclerotic plaques. Immunoreactivity to cytoplasmic  death domain, Fas, and CPP-32, a prominent mediator of apoptosis, was  consistent with the amount of apoptosis detected. Inflammatory cells  and increased number of T-lymphocytes producing apoptotic stimuli could  contribute to plaque instability. The increased levels of proteolytic  activity in atheromatous plaques may make them vulnerable to rupture,  and result in a cascade of thromboembolic cerebrovascular  events.

Molecular Analysis of Factors Contributing to Carotid Atherosclerotic Plaque Instability: Atheromatous versus Fibrous Plaques