Document Detail


Regulation of Na+-H+ exchange in normal NIH-3T3 cells and in NIH-3T3 cells expressing the ras oncogene.
MedLine Citation:
PMID:  2539724     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Our laboratory and others have demonstrated that Na+-H+ exchange can be regulated by two different pathways; one that is mediated by an inositol trisphosphate-stimulated increase in intracellular calcium activity, and one that is mediated by an increase in protein kinase C activity. To determine whether one of these pathways is more important than the other, or whether one pathway is physiologically relevant, we employed normal NIH-3T3 cells (3T3 cells) and NIH-3T3 cells expressing the EJ human bladder ras oncogene (EJ cells). The EJ cells were chosen because they provide a genetic model that does not exhibit serum- or platelet-derived growth factor (PDGF)-stimulated inositol trisphosphate release or Ca2+ mobilization. It was found that serum- or PDGF-stimulated Na+-H+ exchange was more pronounced in EJ cells than in control 3T3 cells. As expected, serum- or PDGF-stimulated Na+-H+ exchange in 3T3 cells was inhibited by chelating intracellular Ca2+ with the intracellular Ca2+ chelator quin2, by the intracellular Ca2+ antagonist 8-(N,N-diethylamino)octyl 3,4,5-trimethoxybenzoate (TMB-8), and by the calmodulin antagonist trifluoperazine. In contrast, these agents did not inhibit serum- or PDGF-stimulated Na+-H+ exchange in EJ cells. Activators of protein kinase C (e.g., 1-oleoyl-2-acetylglycerol or biologically active phorbol esters) were found to stimulate Na+-H+ exchange in EJ cells to the same extent as serum. However, these agents were considerably less effective than serum in control 3T3 cells. Despite these findings, PDGF did not stimulate diacylglycerol levels in EJ cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Authors:
N E Owen; J Knapik; F Strebel; W G Tarpley; R R Gorman
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of physiology     Volume:  256     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1989 Apr 
Date Detail:
Created Date:  1989-05-18     Completed Date:  1989-05-18     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  C756-63     Citation Subset:  IM    
Affiliation:
Department of Biological Chemistry and Structure, University of Health Sciences, Chicago Medical School, Illinois 60064.
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MeSH Terms
Descriptor/Qualifier:
Amiloride / analogs & derivatives,  pharmacology
Aminoquinolines / pharmacology
Animals
Biological Transport
Blood
Calcium / metabolism
Calmodulin / antagonists & inhibitors
Cell Line
Diglycerides / pharmacology
Enzyme Activation / drug effects
Fibroblasts / metabolism*
Gallic Acid / analogs & derivatives,  pharmacology
Genes, ras*
Humans
Inositol Phosphates / metabolism
Mice
Platelet-Derived Growth Factor / pharmacology
Protein Kinase C / metabolism
Protons*
Sodium / metabolism*
Tetradecanoylphorbol Acetate / pharmacology
Transfection
Trifluoperazine / pharmacology
Urinary Bladder
Grant Support
ID/Acronym/Agency:
HL-39159/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Aminoquinolines; 0/Calmodulin; 0/Diglycerides; 0/Inositol Phosphates; 0/Platelet-Derived Growth Factor; 0/Protons; 1154-25-2/ethylisopropylamiloride; 117-89-5/Trifluoperazine; 149-91-7/Gallic Acid; 16561-29-8/Tetradecanoylphorbol Acetate; 2609-46-3/Amiloride; 57818-92-5/8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate; 7440-23-5/Sodium; 7440-70-2/Calcium; 83014-44-2/Quin2; 86390-77-4/1-oleoyl-2-acetylglycerol; EC 2.7.11.13/Protein Kinase C

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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