The nitric oxide donor sodium nitroprusside inhibits mineralization in ATDC5 cells

The aim of this study was to test whether the nitric oxide (NO) donor sodium nitroprusside (SNP) has an effect on mineralization in ATDC5 cells. Mineralization in ATDC5 cell culture was induced by addition of beta-glycerophosphate or inorganic phosphate, visualized by staining precipitated calcium w...

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Bibliographic Details
Published in:Calcified tissue international 2006-03, Vol.78 (3), p.171-177
Main Authors: Huitema, L F A, Vaandrager, A B, van Weeren, P R, Barneveld, A, Helms, J B, van de Lest, C H A
Format: Article
Language:English
Subjects:
Animals
Anthraquinones - metabolism
Apoptosis
Calcification, Physiologic - drug effects
Calcium - analysis
Cell Culture Techniques
Cell Line
Chondrocytes - cytology
Chondrocytes - drug effects
Chondrocytes - metabolism
Dose-Response Relationship, Drug
Histocytochemistry
Mice
Nitric Oxide Donors - pharmacology
Nitroprusside - pharmacology
Phosphates - metabolism
Spectrophotometry, Atomic
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Summary:The aim of this study was to test whether the nitric oxide (NO) donor sodium nitroprusside (SNP) has an effect on mineralization in ATDC5 cells. Mineralization in ATDC5 cell culture was induced by addition of beta-glycerophosphate or inorganic phosphate, visualized by staining precipitated calcium with an alizarin red stain, and quantified using atomic absorption spectrometry. SNP was shown to inhibit the mineralization of ADTC5 cells. This inhibition was not affected by inhibitors of guanylyl cyclase nor mimicked by a cyclic guanosine monophosphate (cGMP) analog. Furthermore, SNP did not inhibit phosphate uptake or inhibit apoptosis in ATDC5 cells. These findings indicate that SNP can specifically inhibit matrix mineralization via a cGMP-independent pathway and that the effect is not mediated by inhibition of phosphate transport or apoptosis. These results suggest a preventive role of NO in premature or pathological mineralization.
ISSN:0171-967X
1432-0827
DOI:10.1007/s00223-005-1233-y