Tenascin-C is associated with coronary plaque instability in patients with acute coronary syndromes
Autor: | Hayashi Yasuhiko, Ueda Hironori, Yamamoto Hideya, Imazu Michinori, Kohno Nobuoki, Kajiwara Kenji |
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Rok vydání: | 2004 |
Předmět: |
Male
medicine.medical_specialty Pathology Myocardial Infarction Coronary Artery Disease Angina Pectoris Pathogenesis Angina Internal medicine Medicine Humans Myocardial infarction Angina Unstable Lymphocytes Aged Neointimal hyperplasia biology business.industry Unstable angina Macrophages Tenascin C Fibrous cap Tenascin General Medicine Middle Aged musculoskeletal system medicine.disease Immunohistochemistry medicine.anatomical_structure biology.protein Cardiology Female Cardiology and Cardiovascular Medicine business Calcification |
Zdroj: | Circulation journal : official journal of the Japanese Circulation Society. 68(3) |
ISSN: | 1346-9843 |
Popis: | Background Tenascin-C (TNC) is an extracellular matrix glycoprotein that increases after inflammation and injury. In cultured cells TNC has been reported to markedly induce the expression of matrix metalloproteinase-9, which stimulates collagen degradation in the fibrous cap of human atherosclerotic plaque. Methods and Results Immunohistochemical techniques were used to analyze the expression of TNC protein in 51 coronary atherectomy specimens obtained from patients with stable angina pectoris (SAP, n=23) or acute coronary syndromes (ACS) (n=28; unstable angina pectoris, n=20, acute myocardial infarction, n=8). Immunostaining for α-smooth muscle actin, CD68, CD45, and CD31 was also performed in serial sections to identify the cell types that express TNC protein. The %TNC + area (percentage of the area of immunostaining for TNC protein in the total surface area of the plaque) was larger in coronary samples with the plaque characteristics of thrombus, angiogenesis, intraplaque hemorrhage, and macrophage (CD68+), and lymphocyte (CD45 +) clusters than in coronary samples without them (52±3.4 vs 39±4.8, p |
Databáze: | OpenAIRE |
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