| Nitric oxide enhances osteoclastogenesis possibly by mediating cell fusion. | |
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MedLine Citation:
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PMID: 19389479 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Osteoclasts are multinucleated bone resorbing cells which form by fusion of pre-osteoclasts. Here, we investigate how nitric oxide (NO) affects osteoclastogenesis. Time lapse photomicrography, using the fluorescent NO indicator dye, 4,5-diaminofluorescein diacetate, revealed an intense NO signal in pre-osteoclasts preceding cell fusion. Osteoclastogenesis in RAW264.7 cells increased when exposed to the NO synthase inhibitor, L-NMMA (0.25 microM), for the initial 48 h. In contrast, pre-osteoclast fusion decreased when RAW264.7 cells were exposed to L-NMMA from 48 to 96 h. Both NO synthase inhibitors, L-NMMA and L-NAME, decreased osteoclast formation during this time period. The inhibitory effect of L-NMMA on osteoclast formation was abolished with increasing concentrations (25-200 ng/ml) of sRANKL suggesting signaling cross talk. NO donors increased osteoclast formation in a dose-dependent manner, with greatest stimulation at 15 microM NOC-12 (2.3 fold) and 5 microM NOC-18 (2.4 fold). Measuring nitrite (NO end product) daily from culture media of RAW264.7 cells undergoing osteoclastogenesis revealed that an increase in NO production coincided with the fusion of pre-osteoclasts (day 4). Inhibiting fusion by plating cells on polystyrene dishes pre-coated with poly-(L-lysine) decreased both osteoclast formation and NO production. To address if NO mediates fusion through the actin cytoskeleton, actin free barbed ends were measured. 0.25 microM L-NMMA decreased, while 15 microM NOC-12 and 5 microM NOC-18 increased actin free barbed ends. We hypothesize that while NO initially negatively regulates pre-osteoclast differentiation; it later facilitates the fusion of mononuclear pre-osteoclasts, possibly by up regulating actin remodeling. |
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Authors:
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Dorrin Nilforoushan; Azza Gramoun; Michael Glogauer; Morris F Manolson |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2009-04-21 |
Journal Detail:
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Title: Nitric oxide : biology and chemistry / official journal of the Nitric Oxide Society Volume: 21 ISSN: 1089-8611 ISO Abbreviation: Nitric Oxide Publication Date: 2009 Aug |
Date Detail:
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Created Date: 2009-07-14 Completed Date: 2009-10-22 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9709307 Medline TA: Nitric Oxide Country: United States |
Other Details:
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Languages: eng Pagination: 27-36 Citation Subset: IM |
Affiliation:
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Faculty of Dentistry, University of Toronto, Toronto, ON, Canada. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acid Phosphatase
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metabolism Actins / metabolism Analysis of Variance Animals Cell Differentiation / drug effects Cell Fusion Cell Line, Tumor Cell Proliferation / drug effects Cell Survival / drug effects Cells, Cultured Enzyme Inhibitors / pharmacology Isoenzymes / metabolism Mice Nitric Oxide / biosynthesis, metabolism* Nitric Oxide Donors / pharmacology Nitric Oxide Synthase / antagonists & inhibitors, metabolism Nitrites / metabolism Nitroso Compounds / pharmacology Osteoclasts / cytology*, drug effects, metabolism* Photomicrography Polylysine / pharmacology Rabbits omega-N-Methylarginine / pharmacology |
| Chemical | |
Reg. No./Substance:
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0/Actins; 0/Enzyme Inhibitors; 0/Isoenzymes; 0/NOC 18; 0/Nitric Oxide Donors; 0/Nitrites; 0/Nitroso Compounds; 10102-43-9/Nitric Oxide; 17035-90-4/omega-N-Methylarginine; 25104-18-1/Polylysine; EC 1.14.13.39/Nitric Oxide Synthase; EC 3.1.3.-/tartrate-resistant acid phosphatase; EC 3.1.3.2/Acid Phosphatase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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