Activation of MAPK by potassium bisperoxo(1,10-phenanthroline)oxovanadate (V)

被引:19
作者
Cerovac, Z
Ban, J
Morinville, A
Yaccato, K
Shaver, A
Maysinger, D
机构
[1] McGill Univ, Dept Pharmacol & Therapeut, Montreal, PQ H3G 1Y6, Canada
[2] Univ Zagreb, Fac Sci, Dept Biol Mol, Zagreb 10000, Croatia
[3] McGill Univ, Dept Chem, Montreal, PQ H3G 1Y6, Canada
基金
加拿大自然科学与工程研究理事会;
关键词
PC12; cells; V-51-NMR; peroxovanadium complexes; JNK; ERK;
D O I
10.1016/S0197-0186(99)00018-2
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Potassium bisperoxo(1,10-phenantroline)oxovanadate (V) [bpV(phen)] is a potent protein tyrocine phosphatase inhibitor which mediates a variety of biological effects. The aim of these studies was to examine the role(s) of mitogen activated protein kinase (MAPK) pathways in PC12 cell proliferation and toxicity by bpV(phen). BpV(phen) exerts a bimodal effect in PC12 cells: proliferation at low and cell death at higher micromolar concentrations. Activation of MAPK by bpV(phen) depends on time and concentration. The phosphorylation pattern of extracellular regulated kinases (ERK 1/2), c-jun N-terminal activated kinases (JNK) and p38 in PC12 cells is strikingly different. Activation of JNK is sustained in PC12 cells. In contrast, ERK 1/2 activation is transient and treatment with PD98059 indicates that ERK activation by bpV(phen) is partly independent from the ras-MEK pathway. Stability studies of bpV(phen) in DMEM and PBS showed linear relationship with T1/2 about 6 h and 10 days in DMEM and PBS, respectively. Comparison between the time courses of MAPK activation and kinetics of bpV(phen) decomposition as assessed by SIV-NMR analysis show that the initial and maximal phosphorylation signals are produced in the presence of the complex bpV(phen) and not caused by the decomposition products of bpV(phen). (C) 1999 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:337 / 344
页数:8
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