Nitric oxide priming protects nitric oxide-mediated apoptosis via HEME OXYGENASE-1 induction

The role of nitric oxide (NO) as a cytotoxic effector molecule of the immune system is clearly established, but recent studies demonstrate cytoprotective functions of NO at low nontoxic concentrations. However, the mechanism of cytoprotection has not been defined completely. Thus, we investigate the...

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Bibliographic Details
Published in:Free radical biology & medicine 2003-05, Vol.34 (9), p.1136-1145
Main Authors: Choi, Byung-Min, Pae, Hyun-Ock, Chung, Hun-Taeg
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Apoptosis - drug effects
Carbon monoxide
Carbon Monoxide - pharmacology
Cell Death - drug effects
Cell Line
Cytoprotection - drug effects
Dose-Response Relationship, Drug
Enzyme Induction - drug effects
Enzyme Inhibitors - pharmacology
Fibroblasts
Free radicals
Heme oxygenase
Heme Oxygenase (Decyclizing) - metabolism
Heme Oxygenase-1
Hemin
Hemin - pharmacology
L929 fibroblast cells
Membrane Proteins
Mice
Nitric oxide
Nitric Oxide - antagonists & inhibitors
Nitric Oxide - metabolism
Nitric Oxide - pharmacology
Nitroprusside - pharmacology
Protoporphyrins - pharmacology
Time Factors
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Summary:The role of nitric oxide (NO) as a cytotoxic effector molecule of the immune system is clearly established, but recent studies demonstrate cytoprotective functions of NO at low nontoxic concentrations. However, the mechanism of cytoprotection has not been defined completely. Thus, we investigate the involvement of heme oxygenase-1 (HO-1) in the cytoprotective effects of NO. Exposure of L929 cells to sodium nitroprusside (SNP) resulted in the induction of HO-1 protein expression and heme oxygenase activity. Pretreatment of the cells with a low dose of NO (200 μM SNP) significantly inhibited a high dose of (1000 μM SNP) NO-induced apoptosis in L929 cells. Cytoprotection by a low dose of NO was abrogated in the presence of the heme oxygenase inhibitor zinc protoporphyrin IX. A cytoprotective effect comparable to a low dose of SNP was observed when the cells were transfected with HO-1 gene or preincubated with another HO-1 inducer, hemin. Additional experiments revealed the involvement of carbon monoxide in the cytoprotective effect of SNP/HO-1 in L929 cells. Our results presented here provide evidence to support the essential role of HO-1 in the cytoprotective function of NO priming.
ISSN:0891-5849
1873-4596
DOI:10.1016/S0891-5849(03)00064-9