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Adenosine Triphosphate Depletion Induces a Rise in Cytosolic Free Calcium in Canine Renal Epithelial Cells

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Adenosine Triphosphate Depletion Induces a Rise in Cytosolic Free Calcium in Canine Renal Epithelial Cells Adenosine triphosphate depletion induces a rise in cytosolic free calcium in canine renal epithelial cells. C E McCoy, … , E A Alexander, J H Schwartz J Clin Invest. 1988;82(4):1326-1332. https://doi.org/10.1172/JCI113734. Research Article An elevation in cytosolic free calcium (Cai) produced by cellular ATP depletion may contribute to the initiation of cytotoxic events in renal ischemia. To evaluate whether ATP depletion results in a rise in Cai we examined the effect of cyanide and 2-deoxy-D-glucose on the Cai of Madin-Darby canine kidney cells. Exposure to the metabolic inhibitors resulted in a rise in Cai from 112 +/- 11 to 649 +/- 99 nM in 15 min. This combination of metabolic inhibitors also resulted in a decrement of cell ATP to 11 +/- 2% of control by 15 min. Experiments that were performed with other metabolic inhibitors confirm that the increment in Cai is due to inhibition of ATP synthesis. With the removal of cyanide and 2-deoxy-D- glucose, Cai recovered to 101 +/- 16 nM. In the absence of extracellular calcium activity (Ca0), Cai declined from 127 +/- 7 to 38 +/- 6 nM, whereas with cyanide plus 2-deoxy-D-glucose in the absence of Ca0 the Cai rose from 108 +/- 21 to 151 +/- 28 nM. Because the rise in Cai produced by ATP depletion in the absence of Ca0 is significantly less than that which occurs in the presence of Ca0, influx of Ca0 is necessary for the maximal rise of Cai. The rise in Cai that occurred in the absence of Ca0 suggests […] Find the latest version: https://jci.me/113734/pdf Adenosine Triphosphate Depletion Induces a Rise in Cytosolic Free Calcium in Canine Renal Epithelial Cells C. E. McCoy, A. M. Selvaggio, E. A. Alexander, and J. H. Schwartz Thorndike Memorial Laboratory, Renal Section, Boston City Hospital and Departments ofMedicine and Physiology, Boston University School ofMedicine, Boston, Massachusetts 02118 Abstract ATP is required to maintain the Ca,. ATP hydrolysis is re- quired to provide energy for the calcium pumps that exist in An elevation in cytosolic free calcium (Cal) produced by cellu- the plasma membrane and the membrane of the endoplasmic lar ATP depletion may contribute to the initiation of cytotoxic reticulum (3). These calcium pumps transport calcium ions events in renal ischemia. To evaluate whether ATP depletion out of the cell and into storage sites within the endoplasmic results in a rise in Cal we examined the effect of cyanide and reticulum. A Na+/Ca++ exchanger exists in the plasma mem- 2-deoxy-D-glucose on the Cal of Madin-Darby canine kidney brane and probably participates in the regulation of Ca, (4). cells. Exposure to the metabolic inhibitors resulted in a rise in Energy is provided by the transcellular sodium gradient that is Ca1 from 112±11 to 649±99 nM in 15 min. This combination maintained by the plasma membrane Na+/K' ATPase. Fi- of metabolic inhibitors also resulted in a decrement of cell ATP nally, calcium is taken up by mitochondria and linked to this to 11±2% of control by 15 min. Experiments that were per- organelle's proton pump (5). Since cellular ATP depletion is formed with other metabolic inhibitors confirm that the incre- the sine qua non of ischemic cellular injury, logic would dic- ment in Ca1 is due to inhibition of ATP synthesis. With the tate that Ca, should rise during ischemia. removal of cyanide and 2-deoxy-D-glucose, Ca1 recovered to An elevated Ca, during cell ischemia could participate in 101±16 nM. In the absence of extracellular calcium activity the pathogenesis of cell injury in several ways. Xanthine dehy- (Cao), Cai declined from 127±7 to 38±6 nM, whereas with drogenase is converted to xanthine oxidase by a calcium-de- cyanide plus 2-deoxy-D-glucose in the absence of Cao the Cal pendent process (1,2). An increased concentration of xanthine rose from 108±21 to 151±28 nM. Because the rise in Cal oxidase could lead to the accumulation of toxic oxygen radi- produced by ATP depletion in the absence of Cao is signifi- cles during reflow. Phospholipases can be activated by a rise in cantly less than that which occurs in the presence of CaO, influx Ca, (6). These enzymes may produce changes in cell mem- of Cao is necessary for the maximal rise of Ca1. The rise in Cai brane permeability and generate potentially cytotoxic fatty that occurred in the absence of Ca. suggests that the release of acids. Calcium has also been shown to accumulate in mito- calcium from intracellular stores contributes to the increment chondria in response to elevations in ambient calcium con- in Ca1 seen with ATP depletion. TMB-8, an inhibitor of cal- centration as well as during ischemia (7-9), a response asso- cium release from intracellular stores, blunted the rise in Ca1 ciated with defects in oxidative phosphorylation (7). Other by nearly 50%. Neither verapamil nor nifedipine inhibited the effects of an elevated Ca, are less well defined but may include rise in Cal. This study demonstrates that ATP depletion in- the activation of calcium-sensitive ion channels (10) and per- duced by the metabolic inhibitors cyanide and 2-deoxy-D-glu- turbations of cytoskeletal components (2). While each of these cose is associated with a rapid and reversible increase in Ca1. events could play an important role in the pathogenesis of Both Cao influx and Cai redistribution contribute to this rise. ischemic cellular injury it has yet to be established whether they do. Introduction Does Ca, rise during cell ischemia? The purpose of these studies was to answer this fundamental question. We chose as It has been proposed that a rise in cytosolic calcium may play a model of cellular ischemia cultured renal epithelial cells an initiating role in the cellular events that lead to epithelial treated with inhibitors of ATP synthesis. We examined the cell injury during ischemic acute renal failure (1, 2). However, effect of ATP depletion on Ca, and the contribution of extra- experimental evidence supporting this hypothesis has been in- cellular calcium (Cao) influx and intracellular redistribution of conclusive. Because the concentration of cytosolic free cal- sequestered calcium. It is clear from our studies that cellular cium (CaJ)' is 10,000-fold less than Cao, energy in the form of ATP depletion induced by metabolic inhibitors is associated with a reversible rise in Ca, Ca, and Cao contribute to this rise. Address all correspondence to Dr. John H. Schwartz, Thordike Labo- ratory 416, Boston City Hospital, 818 Harrison Avenue, Boston, MA Methods 02118. Received for publication 30 July 1987 and in revised form 2 May Cell culture 1988. Madin-Darby canine kidney (MDCK) cells were obtained from Amer- ican Type Tissue Culture (Rockville, MD). Cells were grown in 75-cm2 1. Abbreviations used in this paper: Ca,, cytosolic free calcium; Cao, cell culture flasks (GIBCO, Grand Island, NY). The culture media used extracellular free calcium; MDCK, Madin-Darby canine kidney; was DME (GIBCO) with 10% FCS (HyClone Laboratories, Inc., TMB-8, 3,4,5-trimetoxybenzoate 8-(NN-diethylamino)octyl ester. Logan, UT), 50 ,ug/ml penicillin and 50 jtg/ml streptomycin. Cells were grown in an incubator at 370C and aerated with 95% air and 5% J. Clin. Invest. CO2. For passage, cells were rinsed with a calcium- and magnesium- © The American Society for Clinical Investigation, Inc. free PBS solution. This was followed by exposure to 2 cm3 of 50 mg% 0021-9738/88/10/1326/07 $2.00 trypsin and 20 mg% EGTA in calcium- and magnesium-free Hanks' Volume 82, October 1988, 1326-1332 solution (GIBCO) for 5-15 min. 1326 C. E. McCoy, A. M. Selvaggio, E. A. Alexander, and J. H. Schwartz Cells used for Ca, measurement were passaged to 2.5 cm2 tissue nitrogen (Medical-Technical Gases Inc., Medford, MA) for 30 min culture wells (Costar Corp., Cambridge, MA) containing 12 X 12-mm before and throughout the experimental period. During the experi- glass coverslips. Those cells used in ATP assays were grown in 2.5-cm2 mental period air in the cuvette was replaced by a continuous flow of tissue culture wells without coverslips. Cells were used 48-96 h after nitrogen. passage and after reaching confluence. Study II Cai activity measurement Effect ofcalcium antagonists. Experiments followed a protocol similar MDCK cells were incubated in culture media containing 10 M fura-2 to that in study I except that 50 MM 3,4,5-trimetoxybenzoate 8-NN- acetoxymethylester (Molecular Probes, Eugene, OR) and 0.04% Plur- diethylamino)octyl ester (TMB-8) and/or 1 MM verapamil were added onic F-127 (BASF Corp., Parsippany, NJ) for 1-3 h (11). Fura-2AM during control and experimental periods. To further test the role of and Pluronic F- 127 were prepared as stock solutions in DMSO and the calcium channels, 100MuM verapamil and 10MM nifedipine were used. total DMSO content that the cells were exposed to was < 0.7%. After A higher dose of nifedipine could not be used because of its interfer- fura-2 loading, cells were washed three times with a solution that ence with fura-2 fluorescence. contained 130 mM NaCl, 3.5 mM KCl, 1 mM MgCl, 1 mM CaCl, 1.5 mM KH2PO4, 20 mM Hepes, and 10 mM glucose at a pH of 7.40 Cell A TP measurements (solution A). The coverslip was then placed in a plastic cuvette with a Cells grown in tissue culture wells were treated with solution A con- coverslip holder designed to hold the coverslip at a 350 angle to the taining metabolic inhibitors using the protocol followed for Ca, mea- excitation beam (12).
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