Stress‐activated protein kinase/c‐Jun N‐terminal kinase (JNK) plays a part in endothelin‐1‐induced vascular endothelial growth factor synthesis in osteoblasts

Stress‐activated protein kinase/c‐Jun N‐terminal kinase (JNK) plays a part in endothelin‐1‐induced vascular endothelial growth factor synthesis in osteoblasts
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应激激活蛋白激酶/c-Jun N末端激酶(JNK)在内皮素-1诱导的成骨细胞血管内皮生长因子合成中发挥作用

DOI:
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发表时间:
2002
影响因子:
4
通讯作者:
O. Kozawa
O. Kozawa
中科院分区:
生物学2区
文献类型:
--
作者:
Xiaodan Wang;H. Tokuda;K. Hirade;O. Kozawa

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我们先前报道了内皮素-1(ET-1)激活成骨样MC 3 T3-E1细胞中的p44/p42丝裂原活化蛋白(MAP)激酶和p38 MAP激酶,并且不是p44/p42 MAP激酶而是p38 MAP激酶参与ET-1诱导的血管内皮生长因子(VEGF)合成。在本研究中,我们研究了应激活化蛋白激酶/c-Jun N-末端激酶(JNK)在ET-1诱导的这些细胞中VEGF合成中的参与。在0.1 - 100 nM范围内,ET-1以剂量依赖性方式显著诱导JNK磷酸化。JNK抑制剂SP 600125显著降低ET-1诱导的VEGF合成。SP 600125和SB 203580的组合相加地减少ET-1刺激的VEGF合成。SP 600125可抑制ET-1诱导的JNK磷酸化,但对ET-1诱导的p38 MAP激酶磷酸化无影响。p38 MAP激酶抑制剂SB 203580对ET-1诱导的JNK磷酸化无明显影响。这些结果强烈表明,JNK在成骨细胞中除了p38 MAP激酶外,还在ET-1诱导的VEGF合成中发挥作用。J.细胞。87:417-423,2002.© 2002 Wiley利斯公司
We previously reported that endothelin‐1 (ET‐1) activates both p44/p42 mitogen‐activated protein (MAP) kinase and p38 MAP kinase in osteoblast‐like MC3T3‐E1 cells, and that not p44/p42 MAP kinase but p38 MAP kinase participates in the ET‐1‐induced vascular endothelial growth factor (VEGF) synthesis. In the present study, we investigated the involvement of stress‐activated protein kinase/c‐Jun N‐terminal kinase (JNK) in ET‐1‐induced VEGF synthesis in these cells. ET‐1 significantly induced the phosphorylation of JNK in a dose‐dependent manner in the range between 0.1 and 100 nM. SP600125, an inhibitor of JNK, markedly reduced the ET‐1‐induced VEGF synthesis. A combination of SP600125 and SB203580 additively reduced the ET‐1‐stimulated VEGF synthesis. SP600125 suppressed the ET‐1‐induced phosphorylation of JNK, while having no effect on the phosphorylation of p38 MAP kinase elicited by ET‐1. SB203580, an inhibitor of p38 MAP kinase, hardly affected the ET‐1‐induced phosphorylation of JNK. These results strongly suggest that JNK plays a role in ET‐1‐induced VEGF synthesis in addition to p38 MAP kinase in osteoblasts. J. Cell. Biochem. 87: 417–423, 2002. © 2002 Wiley‐Liss, Inc.
DOI: 10.1210/endo.131.2.1639010
发表时间: 1992-08
期刊: Endocrinology
影响因子: 4.8
作者:
A. Tatrai;Shirley A. Foster;P. Lakatos;G. Shankar;P. Stern
通讯作者: A. Tatrai;Shirley A. Foster;P. Lakatos;G. Shankar;P. Stern
DOI: 10.1210/endo.137.6.8641174
发表时间: 1996-06
期刊: Endocrinology
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
UMR-106 成骨细胞骨肉瘤细胞中内皮素 1 诱发的钙瞬变是通过内皮素 A 和内皮素 B 受体介导的。
DOI: --
发表时间: 1995
期刊: The Journal of pharmacology and experimental therapeutics
影响因子: --
作者:
Semler,DE;Ohlstein,EH;Nambi,P;Slater,C;Stern,PH
通讯作者: Stern,PH