白藜芦醇通过P38和ERK1/2信号通路抑制佛波酯诱导的THP-1细胞中EMMPRIN的表达。
Resveratrol inhibits EMMPRIN expression via P38 and ERK1/2 pathways in PMA-induced THP-1 cells.
作者信息
Huang Zhouqing, Wang Changqian, Wei Li, Wang Jun, Fan Yuqi, Wang Liansheng, Wang Yue, Chen Ting
机构信息
Department of Cardiology, XinHua Hospital, Shanghai Jiaotong University Medical School, 1665 Kongjiang Road, Shanghai 200092, PR China.
出版信息
Biochem Biophys Res Commun. 2008 Sep 26;374(3):517-21. doi: 10.1016/j.bbrc.2008.07.058. Epub 2008 Jul 21.
The extracellular matrix metalloproteinase inducer (EMMPRIN) is significant in the regulation of matrix metalloproteinase (MMP) synthesis in atherosclerosis-related cells, and is possibly involved in the progression of atherosclerotic plaque. EMMPRIN expression is also up-regulated in PMA-induced THP-1 cells and is inhibited by resveratrol. However, it remains unclear how resveratrol inhibits EMMPRIN expression. We thus investigated the role of the MAPK signaling pathway in resveratrol inhibiting the up-regulation of EMMPRIN in PMA-induced THP-1 cells. We found that the ERK1/2 and p38 pathways, but not the JNK, are activated during the up-regulation of EMMPRIN expression. We also observed that while resveratrol suppresses the up-regulation of EMMPRIN, it also suppresses both the ERK1/2 and p38 pathways in a dose-dependent manner. Taken together, we established that it is through both the ERK1/2 and p38 MAPK pathways that resveratrol inhibits the expression of EMMPRIN in PMA-induced THP-1 cells.
细胞外基质金属蛋白酶诱导剂（EMMPRIN）在动脉粥样硬化相关细胞中基质金属蛋白酶（MMP）合成的调节中起重要作用，并且可能参与动脉粥样硬化斑块的进展。在佛波酯（PMA）诱导的THP-1细胞中，EMMPRIN的表达也会上调，且白藜芦醇可抑制其表达。然而，白藜芦醇如何抑制EMMPRIN的表达仍不清楚。因此，我们研究了丝裂原活化蛋白激酶（MAPK）信号通路在白藜芦醇抑制PMA诱导的THP-1细胞中EMMPRIN上调中的作用。我们发现，在EMMPRIN表达上调过程中，细胞外信号调节激酶1/2（ERK1/2）和p38信号通路被激活，而c-Jun氨基末端激酶（JNK）信号通路未被激活。我们还观察到，白藜芦醇在抑制EMMPRIN上调的同时，也以剂量依赖的方式抑制ERK1/2和p38信号通路。综上所述，我们证实白藜芦醇是通过ERK1/2和p38丝裂原活化蛋白激酶信号通路抑制PMA诱导的THP-1细胞中EMMPRIN表达的。
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