| Normotonic cell shrinkage induced by Na+ deprivation results in apoptotic cell death in human epithelial HeLa cells. | |
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MedLine Citation:
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PMID: 16962015 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Miho Nukui; Takahiro Shimizu; Yasunobu Okada |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2006-09-12 |
Journal Detail:
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Title: The journal of physiological sciences : JPS Volume: 56 ISSN: 1880-6546 ISO Abbreviation: J Physiol Sci Publication Date: 2006 Oct |
Date Detail:
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Created Date: 2006-11-02 Completed Date: 2007-03-27 Revised Date: 2008-12-29 |
Medline Journal Info:
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Nlm Unique ID: 101262417 Medline TA: J Physiol Sci Country: Japan |
Other Details:
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Languages: eng Pagination: 335-9 Citation Subset: IM |
Affiliation:
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Department of Cell Physiology, National Institute for Physiological Sciences, Okazaki, 445-8585 Japan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Apoptosis
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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:
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0/Sodium-Calcium Exchanger; 0/Sodium-Hydrogen Antiporter; 0/Sodium-Potassium-Chloride Symporters; 7440-23-5/Sodium |
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