Linked Life Data

15057559

Source:http://linkedlifedata.com/resource/pubmed/id/15057559

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2004-5-17
pubmed:abstractText
K+ and Cl- homeostasis have been implicated in cell volume regulation and apoptosis. We addressed the hypothesis that K+ and Cl- efflux may contribute to apoptotic cell shrinkage and apoptotic death in cultured cortical neurons. CLC-2 and CLC-3 chloride channels were detected in cultured cortical neurons. The Cl- channel blockers 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS), 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid (SITS) and 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB) inhibited the outwardly rectifying Cl- current, prevented apoptotic cell shrinkage, and mildly attenuated cell death induced by staurosporine, C2-ceramide, or serum deprivation. Cl- channel blockers, however, at concentrations that prevented cell shrinkage had no significant effects on caspase activation and/or DNA fragmentation. Cell death in the presence of a Cl- channel blocker was still sensitive to blockade by the caspase inhibitor z-Val-Ala-Asp(OMe)-fluoromethyl ketone (z-VAD-fmk). Electron microscopy revealed that, although DIDS prevented apoptotic cell shrinkage, certain apoptotic ultrastructural alterations still took place in injured neurons. On the other hand, the K+ channel blocker tetraethylammonium (TEA), clofilium, or the caspase inhibitor z-VAD-fmk prevented cell shrinkage as well as caspase activation and/or DNA damage, and showed stronger neuroprotection against apoptotic alterations and cell death. The results indicate that neurons may undergo apoptotic process without cell shrinkage and imply distinct roles for Cl- and K+ homeostasis in regulating different apoptotic events.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0031-6768
pubmed:author
pubmed:copyrightInfo
Copyright 2004 Springer-Verlag
pubmed:issnType
Print
pubmed:volume
448
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
325-34
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:15057559-4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid, pubmed-meshheading:15057559-4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid, pubmed-meshheading:15057559-Animals, pubmed-meshheading:15057559-Apoptosis, pubmed-meshheading:15057559-Caspases, pubmed-meshheading:15057559-Cell Size, pubmed-meshheading:15057559-Cells, Cultured, pubmed-meshheading:15057559-Cerebral Cortex, pubmed-meshheading:15057559-Chloride Channels, pubmed-meshheading:15057559-Enzyme Inhibitors, pubmed-meshheading:15057559-Membrane Potentials, pubmed-meshheading:15057559-Mice, pubmed-meshheading:15057559-Microscopy, Electron, Transmission, pubmed-meshheading:15057559-Neurons, pubmed-meshheading:15057559-Nitrobenzoates, pubmed-meshheading:15057559-Patch-Clamp Techniques, pubmed-meshheading:15057559-Potassium Channel Blockers, pubmed-meshheading:15057559-Potassium Channels
pubmed:year
2004
pubmed:articleTitle
Effects of chloride and potassium channel blockers on apoptotic cell shrinkage and apoptosis in cortical neurons.
pubmed:affiliation
Department of Pathology, Medical University of South Carolina, Charleston, SC 29425, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't