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• W2169731710 abstract "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." @default.
• W2169731710 created "2016-06-24" @default.
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• W2169731710 date "1999-09-01" @default.
• W2169731710 modified "2023-09-27" @default.
• W2169731710 title "Mechanisms contributing to fluid-flow-induced Ca2+ mobilization in articular chondrocytes" @default.
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• W2169731710 doi "https://doi.org/10.1002/(sici)1097-4652(199909)180:3<402::aid-jcp11>3.0.co;2-4" @default.
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