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Nitric Oxide Induces Osteoblast Apoptosis through a Mitochondria‐Dependent Pathway
Author(s) -
HO WEIPIN,
CHEN TALIANG,
CHIU WENTA,
TAI YUTING,
CHEN RUEIMING
Publication year - 2005
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1338.039
Subject(s) - sodium nitroprusside , nitric oxide , osteoblast , cytochrome c , apoptosis , chemistry , mitochondrion , reactive oxygen species , intracellular , microbiology and biotechnology , viability assay , nitric oxide synthase , medicine , endocrinology , biochemistry , biology , in vitro , organic chemistry
A bstract : 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.