Document Detail


Amiloride-sensitive Na+ channels contribute to regulatory volume increases in human glioma cells.
MedLine Citation:
PMID:  17615161     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Despite intensive research, brain tumors remain among the most difficult type of malignancies to treat, due largely to their diffusely invasive nature and the associated difficulty of adequate surgical resection. To migrate through the brain parenchyma and to proliferate, glioma cells must be capable of significant changes in shape and volume. We have previously reported that glioma cells express an amiloride- and psalmotoxin-sensitive cation conductance that is not found in normal human astrocytes. In the present study, we investigated the potential role of this ion channel to mediate regulatory volume increase in glioma cells. We found that the ability of the cells to volume regulate subsequent to cell shrinkage by hyperosmolar solutions was abolished by both amiloride and psalmotoxin 1. This toxin is thought to be a specific peptide inhibitor of acid-sensing ion channel (ASIC1), a member of the Deg/ENaC superfamily of cation channels. We have previously shown this toxin to be an effective blocker of the glioma cation conductance. Our data suggest that one potential role for this conductance may be to restore cell volume during the cell's progression thorough the cell cycle and while the tumor cell migrates within the interstices of the brain.
Authors:
Sandra B Ross; Catherine M Fuller; James K Bubien; Dale J Benos
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2007-07-05
Journal Detail:
Title:  American journal of physiology. Cell physiology     Volume:  293     ISSN:  0363-6143     ISO Abbreviation:  Am. J. Physiol., Cell Physiol.     Publication Date:  2007 Sep 
Date Detail:
Created Date:  2007-09-12     Completed Date:  2007-10-29     Revised Date:  2012-06-08    
Medline Journal Info:
Nlm Unique ID:  100901225     Medline TA:  Am J Physiol Cell Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  C1181-5     Citation Subset:  IM    
Affiliation:
Dept. Physiology and Biophysics, Univ. of Alabama at Birmingham, 1918 University Blvd., MCLM 704, Birmingham, AL 35294-0005, USA. benos@uab.edu
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MeSH Terms
Descriptor/Qualifier:
Amiloride / pharmacology*
Brain Neoplasms / metabolism,  pathology*
Cell Line, Tumor
Glioma / metabolism,  pathology*
Humans
Membrane Potentials / drug effects,  physiology
Osmotic Pressure
Sodium / metabolism
Sodium Channel Blockers / pharmacology*
Sodium Channels / metabolism*
Spider Venoms / pharmacology
Water-Electrolyte Balance / drug effects,  physiology*
Grant Support
ID/Acronym/Agency:
CA-101952/CA/NCI NIH HHS; R01 DK037206/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/PcTX1 protein, Psalmopoeus cambridgei; 0/Sodium Channel Blockers; 0/Sodium Channels; 0/Spider Venoms; 2609-46-3/Amiloride; 7440-23-5/Sodium

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


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