Journal
EUROPEAN JOURNAL OF PHARMACOLOGY
Volume 715, Issue 1-3, Pages 280-285Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.ejphar.2013.05.009
Keywords
Nitric oxide; Ca2+; Apoptosis; TRPV1; S-nitrosylation; Osteoblast
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Funding
- National Natural Science Foundation of China [11204142, 11074133]
- National Basic Research Program of China [2010CB934101]
- International S&T Cooperation Program of China [2011DFA52870]
- Specialized Research Fund for the Doctoral Program of Higher Education [20110031120004]
- 111 Project [B07013]
- Fundamental Research Funds for the Central Universities
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The high-level production of nitric oxide (NO) induced by inflammatory cytokines has been shown to play a key role in the pathogenesis of inflammation-mediated osteoporosis. In the present work, we observed that 1 mM of the NO donor sodium nitroprusside (SNP) induced an increase of the cytosolic calcium concentration ([Ca2+](c)) in osteoblasts, which was completely abolished by applying an extracellular Ca2+-free buffer. Further experiments showed that the SNP-induced [Ca2+](c) increase was specifically blocked by potent antagonists of the transient receptor potential vanilloid subtype 1 (TRPV1) channel: capsazepine, ruthenium red, and La3+ in Ca2+-containing buffer. However, nifedipine, an L-type voltage sensitive Ca2+-channel blocker, failed to suppress the [Ca2+](c) elevation caused by SNP Additionally, 1 mM SNP induced osteoblast apoptosis, which was largely inhibited by the blockers of TRPV1, capsazepine and ruthenium red. Interestingly, our data showed that the SNP-induced [Ca2+](c) increase was significantly inhibited by N-ethylmaleimide, the blocker of S-nitrosylation modification, instead of inhibitors of the NO-cGMP-PKG pathway. Taken together, our data clearly demonstrated that the NO donor SNP resulted in apoptosis associated with TRPV1 channel-mediated Ca2+ entry via S-nitrosylation in osteoblasts. (C) 2013 Elsevier B.V. All rights reserved.
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