Thrombin-, bradykinin-, and arachidonic acid-induced Ca2+ signaling in Ehrlich ascites tumor cells |
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Authors: | Jorgensen, Nanna Koschmieder Petersen, Stine Falsig Hoffmann, Else Kay |
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Abstract: | Stimulation ofsingle Ehrlich ascites tumor cells with agonists (bradykinin, thrombin)and with arachidonic acid (AA) induces increases in the freeintracellular Ca2+ concentration([Ca2+]i)in the presence and absence of extracellularCa2+, measured using theCa2+-sensitive probe fura 2. Sequential stimulation with two agonists elicits sequential increasesin[Ca2+]i,unlike addition of the same agonist twice. Bradykinin and thrombin haveadditive effects on[Ca2+]iin Ca2+-free medium. Thephosphoinositidase C inhibitor U-73122 inhibits the agonist-inducedincreases in[Ca2+]i,whereas ryanodine has no effect. Pretreatment of cells in Ca2+-free medium with thapsigarginabolishes the bradykinin-induced increase in[Ca2+]ibut not the response to thrombin. The AA-induced response is notinhibited by U-73122 and cannot be mimicked by the inactive structuralanalog trifluoromethylarachidonyl ketone. Pretreatment of the cellswith 50 µM AA (but not with 10 µM AA) abolishes the agonist-inducedincrease in[Ca2+]i.Thus bradykinin, thrombin, and AA induce increases in[Ca2+]iin Ehrlich cells due to Ca2+ entryand release from intracellular stores. Thrombin causes release ofCa2+ from an intracellular storethat is insensitive to bradykinin and is not depleted by thapsigarginbut is depleted by AA. |
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