Nitric Oxide Induces Osteoblast Apoptosis through a Mitochondria-Dependent Pathway

: Osteoblasts contribute to bone remodeling. Nitric oxide can regulate osteoblast activities. In this study, we attempted to evaluate the pathophysiological effects of nitric oxide on osteoblasts and its possible mechanism using neonatal rat calvarial osteoblasts as the experimental model. Exposure...

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Bibliographic Details
Published in:Annals of the New York Academy of Sciences 2005-05, Vol.1042 (1), p.460-470
Main Authors: HO, WEI-PIN, CHEN, TA-LIANG, CHIU, WEN-TA, TAI, YU-TING, CHEN, RUEI-MING
Format: Article
Language:English
Subjects:
Activation
Alkaline Phosphatase - metabolism
Animals
Apoptosis
Apoptosis - drug effects
Biocompatibility
Biomedical materials
Bones
Caspase 3
Caspases - metabolism
Cells, Cultured
Cytochromes
Cytochromes c - biosynthesis
Membrane Potentials - drug effects
Mitochondria - drug effects
Mitochondria - metabolism
mitochondrial functions
Mitochondrial Membranes - drug effects
Mitochondrial Membranes - metabolism
Nitric oxide
Nitric Oxide - metabolism
Nitroprusside - pharmacology
osteoblasts
Osteoblasts - cytology
Osteoblasts - drug effects
Osteoblasts - metabolism
Rats
Rats, Wistar
Reactive Oxygen Species - metabolism
Sodium
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Summary:: Osteoblasts contribute to bone remodeling. Nitric oxide can regulate osteoblast activities. In this study, we attempted to evaluate the pathophysiological effects of nitric oxide on osteoblasts and its possible mechanism using neonatal rat calvarial osteoblasts as the experimental model. Exposure of osteoblasts to sodium nitroprusside, a nitric oxide donor, decreased alkaline phosphatase activities and cell viability in a concentration‐ and time‐dependent manner. Apoptotic analysis revealed that sodium nitroprusside time‐dependently increased the percentages of osteoblasts undergoing apoptosis. Administration of sodium nitroprusside reduced the mitochondrial membrane potential of osteoblasts. In parallel with the mitochondrial dysfunction, levels of intracellular reactive oxygen species and cytochrome c were significantly elevated following sodium nitroprusside administration. Exposure of osteoblasts to sodium nitroprusside significantly increased caspase‐3 activity. Results of this study show that nitric oxide, decomposed from sodium nitroprusside, can induce osteoblast apoptosis through a mitochondrion‐dependent cascade that causes mitochondrial dysfunction, release of intracellular reactive oxygen species and cytochrome c from mitochondria to cytoplasm, and activation of caspase‐3.
ISSN:0077-8923
1749-6632
DOI:10.1196/annals.1338.039