Cellular glucose-6-phosphate dehydrogenase (G6PD) status modulates the effects of nitric oxide (NO) on human foreskin fibroblasts

被引：29

作者：

Cheng, ML

Ho, HY

Liang, CM

Chou, YH

Stern, A

Lu, FJ

Chiu, DT ^{[1
]}

机构：

[1] Chang Gung Univ, Grad Inst Basic Med Sci, Tao Yuan, Taiwan

[2] Chang Gung Univ, Sch Med Technol, Tao Yuan, Taiwan

[3] Natl Taiwan Univ, Coll Med, Dept Biochem & Internal Med, Taipei, Taiwan

[4] Acad Sinica, Inst Biol Chem, Taipei, Taiwan

[5] Natl Def Med Ctr, Grad Inst Life Sci, Taipei, Taiwan

[6] Chang Gung Childrens Hosp, Dept Neonatol, Tao Yuan, Taiwan

[7] NYU, Med Ctr, Dept Pharmacol, New York, NY 10016 USA

来源：

FEBS LETTERS | 2000年 / 475卷 / 03期

关键词：

nitric oxide; glucose-6-phosphate dehydrogenase; apoptosis; growth;

D O I：

10.1016/S0014-5793(00)01687-2

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：

Glucose-6-phosphate dehydrogenase (G6PD) plays an important role in cellular redox homeostasis, which is crucial for cell survival. In the present study, we found that G6PD status determines the response of cells exposed to nitric oxide (NO) donor. Treatment with NO donor, sodium nitroprusside (SNP), caused apoptosis in G6PD-deficient human foreskin fibroblasts (HFF1), whereas it was growth stimulatory in the normal counterpart (HFF3). Such effects mere abolished by NO scavengers like hemoglobin. Ectopic expression of G6PD in HFF1 cells switched the cellular response to NO from apoptosis to growth stimulation. Experiments with 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one and 8-bromo-cGMP showed that the effects of NO on HFF1 and HFF3 cells were independent of cGMP signalling pathway. Intriguingly, trolox prevented the SNP-induced apoptosis in HFF1 cells. These data demonstrate that G6PD plays a critical role in regulation of cell growth and survival. (C) 2000 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.

引用

页码：257 / 262

页数：6

共 25 条

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