Document Detail


Normotonic cell shrinkage induced by Na+ deprivation results in apoptotic cell death in human epithelial HeLa cells.
MedLine Citation:
PMID:  16962015     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Apoptosis is a major form of cell death that occurs in response to a variety of signals in both physiological and pathological situations. A hallmark of apoptosis is normotonic cell shrinkage, called apoptotic volume decrease (AVD), the process of which involves fluxes of K(+), Cl(-), and Na(+). Na(+) influx was suggested to be required in Fas-induced apoptosis in human Jurkat T cells, whereas Na(+) efflux was found to be associated with AVD and apoptosis in human HL-60 cells. Here we examined the effects of extracellular Na(+) deprivation on cell volume and viability in human epithelial HeLa cells. The incubation of HeLa cells in normotonic Na(+)-free Ringer solution resulted in persistent cell shrinkage after > or = 30 min and reduction in cell viability after > or = 1 h. After exposure to Na(+)-free solution for 5 h, a marked reduction in cell viability was found to be associated with an activation of caspase-3 without showing significant LDH release, indicating that the cells underwent apoptosis but not necrosis. Na(+) deprivation-induced cell shrinkage and apoptotic cell death were significantly inhibited by a blocker of Na(+)-K(+)-2Cl(-) cotransporter (NKCC) or of the reverse-mode operation of Na(+)/Ca(2+) exchanger (NCX), but not by a blocker of Na(+)/H(+) exchanger (NHE). Therefore it is concluded that Na(+) deprivation causes persistent cell shrinkage resulting from Na(+) efflux mainly via NKCC and NCX and thereafter leads to apoptotic death of HeLa cells. It is also suggested that normotonic cell shrinkage per se, if persistent, provides a sufficient condition for apoptosis induction.
Authors:
Miho Nukui; Takahiro Shimizu; Yasunobu Okada
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-09-12
Journal Detail:
Title:  The journal of physiological sciences : JPS     Volume:  56     ISSN:  1880-6546     ISO Abbreviation:  J Physiol Sci     Publication Date:  2006 Oct 
Date Detail:
Created Date:  2006-11-02     Completed Date:  2007-03-27     Revised Date:  2008-12-29    
Medline Journal Info:
Nlm Unique ID:  101262417     Medline TA:  J Physiol Sci     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  335-9     Citation Subset:  IM    
Affiliation:
Department of Cell Physiology, National Institute for Physiological Sciences, Okazaki, 445-8585 Japan.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis / drug effects*
Cell Size / drug effects
Hela Cells
Humans
Sodium / deficiency*,  pharmacology
Sodium-Calcium Exchanger / metabolism
Sodium-Hydrogen Antiporter / metabolism
Sodium-Potassium-Chloride Symporters / metabolism
Chemical
Reg. No./Substance:
0/Sodium-Calcium Exchanger; 0/Sodium-Hydrogen Antiporter; 0/Sodium-Potassium-Chloride Symporters; 7440-23-5/Sodium

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