Zhang Xincai, Chen Jinqin, Wang Shixun
Department of Cardiology II, Weifang People's Hospital, Kuiwen District, Weifang, Shandong 261041, China.
Department of Sterilization and Supply, Weifang People's Hospital, Kuiwen District, Weifang, Shandong 261041, China.
Biomed Res Int. 2017;2017:4941379. doi: 10.1155/2017/4941379. Epub 2017 May 31.
Atherosclerosis is an important pathological condition which is accompanied by a vascular smooth muscle cell (VSMC) phenotype switch toward a synthetic phenotype. As an acute-phase protein, Serum Amyloid A (SAA) is thought to have a close relationship to atherosclerosis development. However, no study has investigated the direct effect of SAA on the VSMC phenotype switch, as well as the underlying mechanisms. The purpose of our study was to explore the effect of SAA on the VSMC phenotype switch and the potential mechanisms involved. In our study, we found that SAA induced the VSMC phenotype switch which reduced expression of the smooth muscle cell (SMC) marker and enhanced expression of the matrix synthesis related marker. The proliferative ability of VSMCs was also increased by SAA treatment. Furthermore, our research found that SAA activated the ERK1/2 and p38 MAPK signaling pathways. Finally, by applying the ERK1/2 and p38 inhibitors, U0126 and SB203580, we demonstrated that the SAA-induced VSMC phenotype switch was p38-dependent. Taken together, these results indicated that SAA may play an important role in promoting the VSMC phenotype switch through the p38 MAPK signaling pathway.
动脉粥样硬化是一种重要的病理状态，伴随着血管平滑肌细胞（VSMC）表型向合成表型的转变。血清淀粉样蛋白A（SAA）作为一种急性期蛋白，被认为与动脉粥样硬化的发展密切相关。然而，尚无研究探讨SAA对VSMC表型转换的直接影响及其潜在机制。我们研究的目的是探讨SAA对VSMC表型转换的影响及其潜在机制。在我们的研究中，我们发现SAA诱导VSMC表型转换，降低平滑肌细胞（SMC）标志物的表达，增强基质合成相关标志物的表达。SAA处理还增加了VSMC的增殖能力。此外，我们的研究发现SAA激活了ERK1/2和p38 MAPK信号通路。最后，通过应用ERK1/2和p38抑制剂U0126和SB203580，我们证明SAA诱导的VSMC表型转换是p38依赖性的。综上所述，这些结果表明SAA可能通过p38 MAPK信号通路在促进VSMC表型转换中发挥重要作用。
