1993
DOI: 10.1007/bf00966782
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Extracellular ATP stimulates inositol phospholipid turnover and calcium influx in C6 glioma cells

Abstract: Extracellular ATP caused a dose-dependent accumulation of inositol phosphates and a rise in cytosolic free Ca2+ ([Ca2+]i) in C6 glioma cells with an EC50 of 60 +/- 4 and 10 +/- 5 microM, respectively. The threshold concentration of ATP (3 microM) for increasing [Ca2+]i was approximately 10-fold less than that for stimulating phosphoinositide (PI) turnover. The PI response showed a preference for ATP; ADP was about 3-fold less potent than ATP but had a comparable maximal stimulation (11-fold of the control). AM… Show more

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Cited by 24 publications
(19 citation statements)
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“…The phosphorylation of the 85-kDa MARCKS protein was determined autoradiographically as described under "Materials and Methods." and ATP, which are known to be physiological agonists for C6 glioma cells (Lin et al, 1990(Lin et al, , 1992(Lin et al, , 1993 trigger rapid increases in [Ca 2ϩ ] i and that pretreating these cells with 10 nM endothelin-1 or 100 M ATP 2 min before adding TPA prevents the TPA-stimulated PKCs from phosphorylating MARCKS just as did Ca 2ϩ in the BALB/MK keratinocytes of our previous study and ionomycin in the glioma cells of the present study. Thus, Ca 2ϩ ⅐calmodulin appears to be a physiological modulator of MARCKS phosphorylation by PKCs.…”
Section: Discussionsupporting
confidence: 61%
“…The phosphorylation of the 85-kDa MARCKS protein was determined autoradiographically as described under "Materials and Methods." and ATP, which are known to be physiological agonists for C6 glioma cells (Lin et al, 1990(Lin et al, , 1992(Lin et al, , 1993 trigger rapid increases in [Ca 2ϩ ] i and that pretreating these cells with 10 nM endothelin-1 or 100 M ATP 2 min before adding TPA prevents the TPA-stimulated PKCs from phosphorylating MARCKS just as did Ca 2ϩ in the BALB/MK keratinocytes of our previous study and ionomycin in the glioma cells of the present study. Thus, Ca 2ϩ ⅐calmodulin appears to be a physiological modulator of MARCKS phosphorylation by PKCs.…”
Section: Discussionsupporting
confidence: 61%
“…PI hydrolysis was measured as lithium-dependent accumulation of [3HI IPs in cells prelabelled with myo-[3H]inositol, as described previously (Lin and Chuang 1993a). Briefly, confluent cells on 35-mm Petri dishes were labeled with 2.5 gCi/dish of myo-[3H]inositol for 24 h. Labelled cells were then washed and preincubated at 37 ° C for 20 min in physiological saline solution (118 mM NaC1, 4.7 mM KC1, 1.8 mM CaC12, 1.2mM MgC12, 1.2 mM KH2PO4, 11 mM glucose and 20 mM HEPES, pH 7.4) containing 10 mM LiC1.…”
Section: Intact Cellsmentioning
confidence: 99%
“…ATP, NaF and A23187 stimulate PI-PLC via activation of P2u purinoceptors (Lin and Chuang 1993a), G proteins and Ca 2 + influx respectively. Therefore, the common mechanism responsible for the potentiating effects of CaM antagonists is possibly at the PLC level.…”
Section: Intact Cellsmentioning
confidence: 99%
“…Attempts have been made to identify the mechanism of action of ATP on cancer cells and the purinergic receptor subtypes involved. Decreases in cancer cell number may be attributable to an inhibition of cell proliferation mediated via P2Y receptors (Dubyak and De Young 1985;Lin and Chuang 1993;Maaser et al 2002), the stimulation of differentiation with the subsequent inhibition of proliferation via P2X 5 receptors (Cowen et al 1991;Popper and Batra 1993) or the induction of cell death (apoptosis) via P2X 7 receptors (Chueh and Kao 1993). P1 receptors have been described in the human melanoma A375 cell line (Merighi et al 2001), with evidence for all four subtypes of receptor being present, and have been postulated as a possible target for the treatment of this cancer (Merighi et al 2002).…”
Section: Introductionmentioning
confidence: 99%