Document Detail


Dysfunction of regulatory volume increase is a key component of apoptosis.
MedLine Citation:
PMID:  17101138     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Sustained cell shrinkage is a major hallmark of apoptotic cell death. In apoptotic cells, whole cell volume reduction, called apoptotic volume decrease (AVD), proceeds until fragmentation of cells. Under non-apoptotic conditions, human epithelial HeLa cells exhibited a slow regulatory volume increase (RVI) after osmotic shrinkage induced by exposure to hypertonic solution. When AVD was induced by treatment with a Fas ligand, TNF-alpha or staurosporine, however, it was found that HeLa cells failed to undergo RVI. When RVI was inhibited by combined application of Na+/H+ exchanger (NHE) and anion exchanger blockers, hypertonic stress induced prolonged shrinkage followed by caspase-3 activation in HeLa cells. Hypertonicity also induced apoptosis in NHE1-deficient PS120 fibroblasts, which lack the RVI response. When RVI was restored by transfection of these cells with NHE1, hypertonicity-induced apoptosis was completely prevented. Thus, it is concluded that RVI dysfunction is indispensable for the persistence of AVD and induction of apoptosis.
Authors:
Emi Maeno; Nobuyuki Takahashi; Yasunobu Okada
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-11-09
Journal Detail:
Title:  FEBS letters     Volume:  580     ISSN:  0014-5793     ISO Abbreviation:  FEBS Lett.     Publication Date:  2006 Nov 
Date Detail:
Created Date:  2006-11-22     Completed Date:  2007-01-19     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0155157     Medline TA:  FEBS Lett     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  6513-7     Citation Subset:  IM    
Affiliation:
Department of Cell Physiology, National Institute for Physiological Sciences, Okazaki 444-8585, Japan.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis* / drug effects,  genetics
Caspase 3 / metabolism
Cation Transport Proteins / deficiency,  metabolism
Cell Size*
DNA Fragmentation* / drug effects
Enzyme Inhibitors / pharmacology
Fas Ligand Protein / metabolism,  pharmacology
Fibroblasts / cytology,  metabolism*
Hela Cells
Humans
Osmosis / drug effects
Osmotic Pressure / drug effects
Sodium-Hydrogen Antiporter / antagonists & inhibitors,  metabolism
Staurosporine / pharmacology
Tumor Necrosis Factor-alpha / metabolism,  pharmacology
Chemical
Reg. No./Substance:
0/Cation Transport Proteins; 0/Enzyme Inhibitors; 0/Fas Ligand Protein; 0/SLC9A1 protein, human; 0/Sodium-Hydrogen Antiporter; 0/Tumor Necrosis Factor-alpha; 62996-74-1/Staurosporine; EC 3.4.22.-/Caspase 3

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


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