| Effect of glucose on pHin and [Ca2+]in in NIH-3T3 cells transfected with the yeast P-type H(+)-ATPase. | |
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MedLine Citation:
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PMID: 7929598 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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NIH-3T3 cells transfected with yeast H(+)-ATPases (RN1a cells) are tumorigenic (Perona and Serrano, 1988, Nature, 334:438). We have previously shown that RN1a cells maintain a chronically high intracellular pH (pHin) under physiological conditions. We have also shown that RN1a cells are serum-independent for growth, maintain a higher intracellular Ca2+ ([Ca2+]in), and glycolyze more rapidly than their non-transformed counterparts (Gillies et al., Proc. Natl. Acad. Sci., 1990, 87:7414; Gillies et al., Cell. Physiol. Biochem., 1992, 2:159). The present study was aimed to understand the interrelationships between glycolysis, pHin, and [Ca2+]in in RN1a cells and their non-transformed counterparts, NIH-3T3 cells. Our data show that the higher rate of glycolysis observed in RN1a cells is due to the presence of low affinity glucose transporters. Consequently, the higher rate of glycolysis is exacerbated at high glucose concentration in RN1a cells. Moreover, the maximal velocity (Vmax) for glucose utilization is up to sixfold higher in RN1a cells than in the NIH-3T3 cells, suggesting that the number of glucose transporters is higher in RN1a than NIH-3T3 cells. Glucose addition to NIH-3T3 cells results in modest decreases in both pHin and [Ca2+]in. In contrast, RN1a cells respond to glucose with a large decrease in pHin, followed by a large decrease in [Ca2+]in. The decrease in [Ca2+]in observed upon glucose addition is likely due to activation of Ca(2+)-ATPase by glycolysis, since the Ca2+ decrease is abolished by the Ca2+ ATPase inhibitors thapsigargin and cyclopiazonic acid. Glucose addition to ATP-depleted cells results in a decrease in [Ca2+]in, suggesting that ATP furnished by glycolysis is utilized by this pump. |
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Authors:
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G M Martínez; R Martínez-Zaguilán; R J Gillies |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Journal of cellular physiology Volume: 161 ISSN: 0021-9541 ISO Abbreviation: J. Cell. Physiol. Publication Date: 1994 Oct |
Date Detail:
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Created Date: 1994-11-01 Completed Date: 1994-11-01 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 0050222 Medline TA: J Cell Physiol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 129-41 Citation Subset: IM |
Affiliation:
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Department of Biochemistry, University of Arizona, College of Medicine, Tucson 85724. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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3T3 Cells Animals Calcium / metabolism* Calcium-Transporting ATPases / antagonists & inhibitors, metabolism Cell Line, Transformed Glucose / pharmacology* Glycolysis Hydrogen-Ion Concentration Intracellular Membranes / metabolism Mice Osmolar Concentration Proton-Translocating ATPases / antagonists & inhibitors, classification, genetics* Sodium-Hydrogen Antiporter / antagonists & inhibitors Transfection* Yeasts / enzymology, genetics* |
| Grant Support | |
ID/Acronym/Agency:
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R01 GM43046-01/GM/NIGMS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Sodium-Hydrogen Antiporter; 50-99-7/Glucose; 7440-70-2/Calcium; EC 3.6.1.8/Calcium-Transporting ATPases; EC 3.6.3.14/Proton-Translocating ATPases |
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