Increased ubiquitin immunoreactivity in unstable atherosclerotic plaques associated with acute coronary syndromes

Joerg Herrmann, William D. Edwards, David Holmes, Kris L. Shogren, Lilach O Lerman, Aaron Ciechanover, Amir Lerman

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Abstract

OBJECTIVES: The current study was designed to examine whether ubiquitin expression is higher in unstable than in stable lesions of patients with acute coronary syndrome (ACS). 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 patients with fatal ACS. Lesions of both infarct-related and noninfarct-related segments from the same patients were examined for the expression and localization of ubiquitin by use of immunohistochemistry and a semiquantitative grading scale. RESULTS: Ubiquitin immunoreactivity was higher in infarct-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 neointima cells and media smooth muscle cells. CONCLUSIONS: In patients with ACS, ubiquitin immunoreactivity is enhanced in unstable, infarct-related lesions, predominantly in plaque regions of tissue degradation. Based on these findings, this study suggests a role for the ubiquitin system in the destabilizadon and rupture of coronary atherosclerotic plaques in humans.

Original languageEnglish (US)
Pages (from-to)1919-1927
Number of pages9
JournalJournal of the American College of Cardiology
Volume40
Issue number11
DOIs
StatePublished - Dec 4 2002

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Atherosclerotic Plaques
Acute Coronary Syndrome
Ubiquitin
Rupture
Neointima
Proteolysis
Smooth Muscle Myocytes
Autopsy
Immunohistochemistry
Macrophages
T-Lymphocytes
Lipids

ASJC Scopus subject areas

  • Nursing(all)

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Increased ubiquitin immunoreactivity in unstable atherosclerotic plaques associated with acute coronary syndromes. / Herrmann, Joerg; Edwards, William D.; Holmes, David; Shogren, Kris L.; Lerman, Lilach O; Ciechanover, Aaron; Lerman, Amir.

In: Journal of the American College of Cardiology, Vol. 40, No. 11, 04.12.2002, p. 1919-1927.

Research output: Contribution to journalArticle

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abstract = "OBJECTIVES: The current study was designed to examine whether ubiquitin expression is higher in unstable than in stable lesions of patients with acute coronary syndrome (ACS). 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 patients with fatal ACS. Lesions of both infarct-related and noninfarct-related segments from the same patients were examined for the expression and localization of ubiquitin by use of immunohistochemistry and a semiquantitative grading scale. RESULTS: Ubiquitin immunoreactivity was higher in infarct-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 neointima cells and media smooth muscle cells. CONCLUSIONS: In patients with ACS, ubiquitin immunoreactivity is enhanced in unstable, infarct-related lesions, predominantly in plaque regions of tissue degradation. Based on these findings, this study suggests a role for the ubiquitin system in the destabilizadon and rupture of coronary atherosclerotic plaques in humans.",
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