(−)‐epigallocatechin gallate enhances prostaglandin F2α‐induced VEGF synthesis via upregulating SAPK/JNK activation in osteoblasts
(−)‐epigallocatechin gallate enhances prostaglandin F2α‐induced VEGF synthesis via upregulating SAPK/JNK activation in osteoblasts
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(−)-表没食子儿茶素没食子酸酯通过上调成骨细胞中 SAPK/JNK 活化增强前列腺素 F2α 诱导的 VEGF 合成
DOI：
10.1002/jcb.21104
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发表时间：
2007
影响因子：
4
通讯作者：
O. Kozawa
中科院分区：
文献类型：
--
作者：
H. Tokuda;S. Takai;R. Matsushima;Shigeru Akamatsu;Y. Hanai;T. Hosoi;A. Harada;T. Ohta;O. Kozawa
儿茶素是茶叶等植物中的主要类黄酮之一，据报道可抑制骨吸收。我们先前报道了前列腺素F2 α（PGF2 α）通过p44/p42丝裂原活化蛋白（MAP）激酶刺激成骨样MC3T3-E1细胞合成血管内皮生长因子（VEGF）。为了阐明儿茶素对成骨细胞的作用机制，我们研究了主要的绿色茶黄酮之一（-）-表没食子儿茶素没食子酸酯（EGCG）对MC3T3-E1细胞中PGF 2 α合成VEGF的影响。EGCG显著增强PGF 2 α诱导的VEGF合成。在10至100 µ M之间，EGCG的放大效应具有剂量依赖性。EGCG不影响PGF 2 α诱导的p44/p42 MAP激酶磷酸化。p38 MAP激酶特异性抑制剂SB 203580和应激活化蛋白激酶/c-Jun N-末端激酶（SAPK/JNK）特异性抑制剂SP 600125可减少PGF 2 α诱导的VEGF合成。EGCG显著增强PGF 2 α诱导的SAPK/JNK磷酸化，而不影响PGF 2 α诱导的p38 MAP激酶磷酸化。SP600125显著降低EGCG对SAPK/JNK磷酸化的扩增。此外，EGCG可扩增PGF 2 α诱导的c-Jun磷酸化。这些结果强烈表明，EGCG上调PGF 2 α刺激的VEGF合成，这是由于成骨细胞中SAPK/JNK的激活增强。J.细胞。100：1146 - 1153，2007.© 2006 Wiley利斯公司
Catechin, one of the major flavonoids presented in plants such as tea, reportedly suppresses bone resorption. We previously reported that prostaglandin F2α (PGF2α) stimulates the synthesis of vascular endothelial growth factor (VEGF) via p44/p42 mitogen‐activated protein (MAP) kinase in osteoblast‐like MC3T3‐E1 cells. To clarify the mechanism of catechin effect on osteoblasts, we investigated the effect of (−)‐epigallocatechin gallate (EGCG), one of the major green tea flavonoids, on the VEGF synthesis by PGF2α in MC3T3‐E1 cells. The PGF2α‐induced VEGF synthesis was significantly enhanced by EGCG. The amplifying effect of EGCG was dose dependent between 10 and 100 µM. EGCG did not affect the PGF2α‐induced phosphorylation of p44/p42 MAP kinase. SB203580, a specific inhibitor of p38 MAP kinase, and SP600125, a specific inhibitor of stress‐activated protein kinase/c‐Jun N‐terminal kinase (SAPK/JNK), reduced the PGF2α‐induced VEGF synthesis. EGCG markedly enhanced the phosphorylation of SAPK/JNK induced by PGF2α without affecting the PGF2α‐induced phosphorylation of p38 MAP kinase. SP600125 markedly reduced the amplification by EGCG of the SAPK/JNK phosphorylation. In addition, the PGF2α‐induced phosphorylation of c‐Jun was amplified by EGCG. These results strongly suggest that EGCG upregulate PGF2α‐stimulated VEGF synthesis resulting from amplifying activation of SAPK/JNK in osteoblasts. J. Cell. Biochem. 100: 1146–1153, 2007. © 2006 Wiley‐Liss, Inc.
影响因子：
4.8
作者：
D. Goad;J. Rubin;Hong Wang;A. Tashjian;C. Patterson
通讯作者：
D. Goad;J. Rubin;Hong Wang;A. Tashjian;C. Patterson