Kenji Kajiwara, Hironori Ueda, Hideya Yamamoto, Michinori Imazu, Yasuhiko Hayashi, Nobuoki Kohno
Department of Molecular and Internal Medicine, Graduate School of Biochemical Sciences, Hiroshima University, Japan.
Circ J. 2004 Mar;68(3):198-203. doi: 10.1253/circj.68.198.
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.
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 alpha-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<0.05; 57+/-3.7 vs 36+/-3.7, p<0.01; 51+/-3.6 vs 39+/-4.8, p<0.05; 53+/-3.4 vs 33+/-4.5, p<0.01; 56+/-4.1 vs 37+/-3.6, p<0.01, respectively). The presence of other components, such as dense fibrous tissue, neointimal hyperplasia, atheromatous gruel and calcification, was not significantly correlated with the %TNC + area. The %TNC + area was larger in coronary samples from patients with ACS than in samples from patients with SAP (56+/-3.2% vs 34+/-4.3%, p<0.01).
The results suggest that TNC may have specific functions in coronary plaque formation and may be involved in the pathogenesis of coronary lesions in ACS.
腱生蛋白-C（TNC）是一种细胞外基质糖蛋白，在炎症和损伤后会增加。在培养细胞中，据报道TNC可显著诱导基质金属蛋白酶-9的表达，该酶可刺激人类动脉粥样硬化斑块纤维帽中的胶原蛋白降解。
采用免疫组织化学技术分析了51例冠状动脉斑块切除标本中TNC蛋白的表达情况，这些标本取自稳定型心绞痛（SAP，n = 23）或急性冠状动脉综合征（ACS）（n = 28；不稳定型心绞痛，n = 20，急性心肌梗死，n = 8）患者。还对连续切片进行了α-平滑肌肌动蛋白、CD68、CD45和CD31的免疫染色，以识别表达TNC蛋白的细胞类型。与无血栓、血管生成、斑块内出血以及巨噬细胞（CD68(+)）和淋巴细胞（CD45(+)）聚集等斑块特征的冠状动脉样本相比，具有这些特征的冠状动脉样本中TNC +面积百分比（TNC蛋白免疫染色面积在斑块总表面积中所占的百分比）更大（分别为52±3.4对39±4.8，p<0.05；57±3.7对36±3.7，p<0.01；51±3.6对39±4.8，p<0.05；53±3.4对33±4.5，p<0.01；56±4.1对37±3.6，p<0.01）。其他成分，如致密纤维组织、新生内膜增生、粥样粥状物和钙化的存在与TNC +面积百分比无显著相关性。ACS患者冠状动脉样本中的TNC +面积百分比大于SAP患者样本中的（56±3.2%对34±4.3%，p<0.01）。
结果表明，TNC可能在冠状动脉斑块形成中具有特定功能，且可能参与ACS冠状动脉病变的发病机制。
