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Mechanisms contributing to fluid‐flow‐induced Ca2+ mobilization in articular chondrocytes

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 ([Ca2+]i). However, the mechanism by which Ca2+ is mobilized in response to flow is unclear. In this study, we investigated the roles of intracellular Ca2+ stores, G‐proteins, and extracellular ATP in the flow‐induced Ca2+ response in bovine articular chondrocytes (BAC). Cells loaded with the Ca2+ sensitive dye Fura‐2 were exposed to steady flow at 34 ml/min (37 dynes/cm2) in a parallel plate flow chamber. Whereas ryanodine and caffeine had no effect, both neomycin and thapsigargin significantly decreased the Ca2+i response to flow, suggesting a role for Ca2+ store release, possibly through an inositol 1,4,5‐trisphosphate (IP3)‐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 Ca2+ 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 IP3 stimulated Ca2+i release and G‐protein activation. J. Cell. Physiol. 180:402–408, 1999. © 1999 Wiley‐Liss, Inc.