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Mechanisms contributing to fluid‐flow‐induced Ca 2+ mobilization in articular chondrocytes
Author(s) -
Yellowley Clare E.,
Jacobs Christopher R.,
Donahue Henry J.
Publication year - 1999
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/(sici)1097-4652(199909)180:3<402::aid-jcp11>3.0.co;2-4
Subject(s) - thapsigargin , extracellular , intracellular , pertussis toxin , chemistry , calcium , ryanodine receptor , microbiology and biotechnology , inositol trisphosphate , calcium in biology , biophysics , inositol , g protein , biochemistry , biology , signal transduction , receptor , organic chemistry
We previously showed that fluid flow, which chondrocytes experience in vivo and which results in a variety of morphological and metabolic changes in cultured articular chondrocytes, can also stimulate a rise in intracellular calcium concentration ([Ca 2+ ] i ). However, the mechanism by which Ca 2+ is mobilized in response to flow is unclear. In this study, we investigated the roles of intracellular Ca 2+ stores, G‐proteins, and extracellular ATP in the flow‐induced Ca 2+ response in bovine articular chondrocytes (BAC). Cells loaded with the Ca 2+ sensitive dye Fura‐2 were exposed to steady flow at 34 ml/min (37 dynes/cm 2 ) in a parallel plate flow chamber. Whereas ryanodine and caffeine had no effect, both neomycin and thapsigargin significantly decreased the Ca 2+ i response to flow, suggesting a role for Ca 2+ store release, possibly through an inositol 1,4,5‐trisphosphate (IP 3 )‐dependent mechanism. Twenty‐four‐hour treatment with pertussis toxin also significantly decreased the response, suggesting that the mechanism may be G‐protein regulated. In addition, ATP release by chondrocytes does not appear to mediate the flow‐induced Ca 2+ response because suramin, a P2 purinergic blocker, had no effect. These results suggest that BAC respond rapidly to changes in their mechanical environment, such as increased fluid flow, by a mechanism that involves IP 3 stimulated Ca 2+ i release and G‐protein activation. J. Cell. Physiol. 180:402–408, 1999. © 1999 Wiley‐Liss, Inc.