Journal
OSTEOARTHRITIS AND CARTILAGE
Volume 11, Issue 3, Pages 187-197Publisher
W B SAUNDERS CO LTD
DOI: 10.1053/S1063-4584(02)00347-3
Keywords
chondrocyte; cartilage; F-actin; Ca2+ osteoarthritis; gelsolin; inositol trisphosphate; osmotic
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Funding
- NIAMS NIH HHS [AR39162, AR43876] Funding Source: Medline
- NIA NIH HHS [AG15768] Funding Source: Medline
- NIGMS NIH HHS [GM08555] Funding Source: Medline
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Objective: The aim of this study was to investigate the effects of hypo-osmotically induced calcium (Ca2+) transients on the organization of the actin cytoskeleton in articular chondrocytes. The secondary hypothesis tested was that actin restructuring following hypo-osmotic stress is mediated by gelsolin. Methods: Isolated porcine chondrocytes were exposed to hypo-osmotic stress, and [Ca2+](i) was monitored using laser scanning microscopy. Calcium transients were monitored using fluorescent ratiometric imaging. The intracellular distribution of actin was examined using fluorescent immunohistochemistry and transient transfection with the pEGFP-actin plasmid. The intracellular distribution of gelsolin was investigated using fluorescent immunohistochemistry. Results: Osmotic stress induced transient increases in [Ca2+](i) caused reorganization of intracellular actin through a mechanism that required Ca2+ in the extracellular media. Fluorescence microscopy revealed that gelsolin was colocalized with F-actin immediately following hypo-osmotic stress but dissociated over time. Conclusion: These results indicate that hypo-osmotic stress induces a gelsolin-mediated reorganization of actin through a transient increase in [Ca2+](i). (C) 2003 OsteoArthritis Research Society International. Published by Elsevier Science Ltd. All rights reserved.
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