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Article: Role of Protein Kinase C in Acidosis Induced Glial Swelling - Current Understanding

TitleRole of Protein Kinase C in Acidosis Induced Glial Swelling - Current Understanding
Authors
Issue Date1997
Citation
Acta Neurochirurgica, Supplement, 1997, v. 1997 n. 70, p. 225-227 How to Cite?
AbstractA major factor in secondary brain injury following cerebral trauma is accumulation of lactic acid resulting in glial swelling. Further, evidence obtained in this context demonstrates activation of protein kinase C (PKC) under these circumstances. Glial swelling from acidosis is attributable to activation of the Na+/H+-exchanger, mediating influx of Na+-ions in exchange for the extrusion of H+ ions. The antiporter is activated following phosphorylation by PKC. The current study was made to elucidate the role of PKC activation in acidosis-induced glial swelling. For that purpose, suspended C6 glioma cells were used to examine changes of the cell volume and intracellular pH (pHi). Acidosis was induced by administration of isotonic lactic acid. Stimulation of PKC by the phorbolester PMA was significantly enhancing glial swelling from severe acidosis (pH 6.2), whereas the decrease of pH1 was somewhat attenuated. On the other side, inhibition of PKC by staurosporine did not affect cell swelling nor the decrease of pH, from acidosis. The results indicate that activation of PKC in cerebral trauma or ischemia may enhance glial swelling from lactacidosis.
Persistent Identifierhttp://hdl.handle.net/10722/149566
ISSN
2015 SCImago Journal Rankings: 0.379
References

 

DC FieldValueLanguage
dc.contributor.authorChang, RCCen_US
dc.contributor.authorPlesnila, Nen_US
dc.contributor.authorRingel, Fen_US
dc.contributor.authorGrönlinger, Cen_US
dc.contributor.authorStaub, Fen_US
dc.contributor.authorBaethmann, Aen_US
dc.date.accessioned2012-06-26T05:55:21Z-
dc.date.available2012-06-26T05:55:21Z-
dc.date.issued1997en_US
dc.identifier.citationActa Neurochirurgica, Supplement, 1997, v. 1997 n. 70, p. 225-227en_US
dc.identifier.issn0065-1419en_US
dc.identifier.urihttp://hdl.handle.net/10722/149566-
dc.description.abstractA major factor in secondary brain injury following cerebral trauma is accumulation of lactic acid resulting in glial swelling. Further, evidence obtained in this context demonstrates activation of protein kinase C (PKC) under these circumstances. Glial swelling from acidosis is attributable to activation of the Na+/H+-exchanger, mediating influx of Na+-ions in exchange for the extrusion of H+ ions. The antiporter is activated following phosphorylation by PKC. The current study was made to elucidate the role of PKC activation in acidosis-induced glial swelling. For that purpose, suspended C6 glioma cells were used to examine changes of the cell volume and intracellular pH (pHi). Acidosis was induced by administration of isotonic lactic acid. Stimulation of PKC by the phorbolester PMA was significantly enhancing glial swelling from severe acidosis (pH 6.2), whereas the decrease of pH1 was somewhat attenuated. On the other side, inhibition of PKC by staurosporine did not affect cell swelling nor the decrease of pH, from acidosis. The results indicate that activation of PKC in cerebral trauma or ischemia may enhance glial swelling from lactacidosis.en_US
dc.languageengen_US
dc.relation.ispartofActa Neurochirurgica, Supplementen_US
dc.subject.meshAcidosis, Lactic - Physiopathologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBrain Injuries - Pathology - Physiopathologyen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshCell Size - Physiologyen_US
dc.subject.meshEnzyme Activationen_US
dc.subject.meshNeuroglia - Pathologyen_US
dc.subject.meshProtein Kinase C - Drug Effects - Physiologyen_US
dc.subject.meshTetradecanoylphorbol Acetate - Pharmacologyen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.titleRole of Protein Kinase C in Acidosis Induced Glial Swelling - Current Understandingen_US
dc.typeArticleen_US
dc.identifier.emailChang, RCC:rccchang@hkucc.hku.hken_US
dc.identifier.authorityChang, RCC=rp00470en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid9416329-
dc.identifier.scopuseid_2-s2.0-0031300332en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031300332&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume1997en_US
dc.identifier.issue70en_US
dc.identifier.spage225en_US
dc.identifier.epage227en_US
dc.publisher.placeAustriaen_US
dc.identifier.scopusauthoridChang, RCC=7403713410en_US
dc.identifier.scopusauthoridPlesnila, N=7003609441en_US
dc.identifier.scopusauthoridRingel, F=6602136569en_US
dc.identifier.scopusauthoridGrönlinger, C=6507376965en_US
dc.identifier.scopusauthoridStaub, F=7006611117en_US
dc.identifier.scopusauthoridBaethmann, A=7004994793en_US

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