Document Detail


Cell volume regulatory ion channels in cell proliferation and cell death.
MedLine Citation:
PMID:  17875419     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Alterations of cell volume are key events during both cell proliferation and apoptotic cell death. Cell proliferation eventually requires an increase of cell volume, and apoptosis is typically paralleled by cell shrinkage. Alterations of cell volume require the participation of ion transport across the cell membrane, including appropriate activity of Cl(-) and K(+) channels. Cl(-) channels modify cytosolic Cl(-) activity and mediate osmolyte flux, and thus influence cell volume. Most Cl(-) channels allow exit of HCO(3)(-), leading to cytosolic acidification, which in turn inhibits cell proliferation and favors apoptosis. K(+) exit through K(+) channels decreases cytosolic K(+) concentration, which may sensitize the cell for apoptotic cell death. K(+) channel activity further maintains the cell membrane potential, a critical determinant of Ca(2+) entry through Ca(2+) channels. Ca(2+) may, in addition, enter through Ca(2+)-permeable cation channels, which, in some cells, are activated by hyperosmotic shock. Increases of cytosolic Ca(2+) activity may trigger both mechanisms required for cell proliferation and mechanisms, leading to apoptosis. Thereby cell proliferation and apoptosis depend on magnitude and temporal organization of Ca(2+) entry, as well as activity of other signaling pathways. Accordingly, the same ion channels may participate in the stimulation of both cell proliferation and apoptosis. Specific ion channel blockers may thus abrogate both cellular mechanisms, depending on cell type and condition.
Authors:
Florian Lang; Michael Föller; Karl Lang; Philipp Lang; Markus Ritter; Alexey Vereninov; Ildiko Szabo; Stephan M Huber; Erich Gulbins
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Methods in enzymology     Volume:  428     ISSN:  0076-6879     ISO Abbreviation:  Meth. Enzymol.     Publication Date:  2007  
Date Detail:
Created Date:  2007-09-18     Completed Date:  2007-11-05     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0212271     Medline TA:  Methods Enzymol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  209-25     Citation Subset:  IM    
Affiliation:
Department of Physiology, University of Tübingen, Germany.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / physiology*
Calcium Channels / physiology
Cell Proliferation*
Cell Size*
Chloride Channels / physiology
Humans
Hydrogen-Ion Concentration
Ion Channels / physiology*
Potassium Channels / physiology
Voltage-Dependent Anion Channels / physiology
Chemical
Reg. No./Substance:
0/Calcium Channels; 0/Chloride Channels; 0/Ion Channels; 0/Potassium Channels; 0/Voltage-Dependent Anion Channels

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


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