Increased ubiquitin immunoreactivity in unstable atherosclerotic plaques associated with XXXX .

@entity1 @entity1187 @entity4798 @entity1188 @entity453 @entity8233
OBJECTIVES: The current study was designed to examine whether ubiquitin expression is higher in unstable than in stable lesions of @entity1 with @entity1187 ( @entity1187 ). BACKGROUND: The ubiquitin system has been identified as the nonlysosomal pathway of protein degradation; it is involved in a number of biologic processes crucial to cell and tissue integrity and therefore, might be potentially involved in the rupture of unstable coronary plaques. METHODS: We conducted an autopsy-based study of 25 consecutive @entity1 with fatal @entity1187 . Lesions of both @entity1188 -related and noninfarct-related segments from the same @entity1 were examined for the expression and localization of ubiquitin by use of immunohistochemistry and a semiquantitative grading scale. RESULTS: Ubiquitin immunoreactivity was higher in @entity1188 -related than in noninfarct-related lesions (1.4 +/- 0.5 vs. 1.1 +/- 0.6, p = 0.03). Compared with areas adjacent to the plaque (0.6 +/- 0.7), ubiquitin immunoreactivity was higher in areas around the lipid core (2.5 +/- 0.8, p < 0.001), plaque shoulders (1.6 +/- 1.1, p < 0.001), and fibrous cap regions (1.6 +/- 1.1, p < 0.001). Within the plaque area, co-localization of ubiquitin immunoreactivity with T cells and macrophages was found. In areas adjacent to the plaque, ubiquitin immunoreactivity co-localized with @entity8233 cells and media smooth muscle cells. CONCLUSIONS: In @entity1 with @entity1187 , ubiquitin immunoreactivity is enhanced in unstable, @entity4798 , predominantly in plaque regions of tissue degradation. Based on these findings, this study suggests a role for the ubiquitin system in the destabilization and rupture of @entity453 in @entity1 .
