Significant expression of endoglin (CD105), TGFβ-1 and TGFβR-2 in the atherosclerotic aorta: An immunohistological study

Department of Pathology and Biodefense, Saga University Faculty of Medicine, Saga 849-8501, Japan.
Journal of atherosclerosis and thrombosis (Impact Factor: 2.73). 04/2006; 13(2):82-9.
Source: PubMed


To date, the glycoprotein endoglin and its receptor complex, formed between TGFbeta and TGFbeta R-2, have been studied in tumor angiogenesis. The purpose of this study is to investigate the expression profile of endoglin and its receptor complex in human atherosclerotic lesions, and compare it to that in non-atherosclerotic tissues. Twenty-six atherosclerotic lesions and twenty-six non-atherosclerotic aortic tissues were collected from thirty-six autopsy cases. Indirect immunohistochemical staining was performed to detect the presence of endoglin, TGFbeta-1, and TGFbeta R-2 proteins in aortic tissues. Endoglin expression was observed in smooth muscle cells (SMC), macrophages and endothelial cells of aortic atherosclerotic lesions. The levels of TGFbeta-1 and TGFbeta R-2 were increased in the intimal matrices, smooth muscle cells, and macrophages, as well as in endothelial cells. The expression levels of endoglin, TGFbeta-1, and TGFbeta R-2 were higher in atherosclerotic lesions than in non-atherosclerotic aortic tissues (p < 0.0001), and there was a correlation among the expression of endoglin, TGFbeta-1, and TGFbeta R-2 in atherosclerotic aortic lesions (p < 0.001). Endoglin or its receptor complex may participate in the atherogenesis.

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