Genistein suppresses smooth muscle cell-derived foam cell formation through tyrosine kinase pathway
Genistein suppresses smooth muscle cell-derived foam cell formation through tyrosine kinase pathway
复制标题
金雀异黄素通过酪氨酸激酶途径抑制平滑肌细胞衍生的泡沫细胞形成。
DOI：
10.1016/j.bbrc.2015.04.155
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发表时间：
2015-08-07
影响因子：
3.1
通讯作者：
Zhang, Liming
中科院分区：
文献类型：
--
作者：
Lin, Jinghan;Xu, Yi;Zhang, Liming
Purpose: Genistein, as a protein tyrosine kinase inhibitor, has been shown to possess anti-atherosclerotic effects. Since the smooth muscle cell-derived foam cells are key components of atherosclerotic plaques. The aim of this study is to investigate the influence of genistein on foam cell transformation from vascular smooth muscle cells and possible mechanisms contributing to these effects.Methods and Results: Vascular smooth muscle cells exposed to ox-LDL developed into foam cell, as demonstrated by Oil Red 0 staining and cholesterol content analysis. Ox-LDL induced phenotype transformation of smooth muscle cells, decreased expression of alpha-actin and increased expression of CD68 (a specific marker for monocytes, can also function as a subtype of scavenger receptors). The expression of scavenger receptors CD36 and LOX-1 was measured, and their role in foam cell formation in the presence of genistein, daidzein (a structurally similar analogue of genistein) and herbimycin A (a commonly tyrosine kinase inhibitor). The results showed that foam cell formation was markedly reduced by genistein and herbimycin A, as well as the expression of CD68, CD36 and LOX-1. However, daidzein had no such effect. In addition, genistein-induced down-regulation of CD68, CD36 and LOX-1 could be reversed by sodium orthovanadate (a membrane-permeable protein tyrosine phosphatase inhibitor).Conclusion: The results showed that ox-LDL induce smooth muscle cell-derived foam cell formation and transform the phenotype of smooth muscle cell. While tyrosine kinase inhibitor, genistein could suppress smooth muscle cell-derived foam cell formation through inhibiting the protein expressions of CD68, CD36 and LOX-1. (C) 2015 Elsevier Inc. All rights reserved.
