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dc.contributor.authorMartinus, Ryan Dennis
dc.contributor.authorCook, Christian
dc.coverage.spatialEnglanden_NZ
dc.date.accessioned2011-07-19T23:07:15Z
dc.date.available2011-07-19T23:07:15Z
dc.date.issued2011-08
dc.identifier.citationMartinus, R. & Cook, C. (2011). The effect of complement C5a on mitochondrial functions of PC12 cells. Neuroreport, 22(2), 581-585.en_NZ
dc.identifier.urihttps://hdl.handle.net/10289/5494
dc.description.abstractC5a is thought to play a role during complement-activated neuronal apoptotic cell death in the central nervous system. The mechanisms responsible are however not well-understood. As mitochondria play a key role during apoptosis, we investigated mitochondria as a potential target for C5a. Using PC12 cells, we demonstrated that exposure to C5a led to inhibition of mitochondrial respiration, dehydrogenase and cytochrome c oxidase activities. Interestingly, an increase in expression of the mitochondrial stress protein chaperonin 60 was also observed, confirming a marked effect of C5a on mitochondrial functions. These observations are the first documented intracellular effects noted for the complement molecule C5a in in-vitro cultured cells.en_NZ
dc.language.isoen
dc.publisherLippincott Williams & Wilkinsen_NZ
dc.relation.urihttp://journals.lww.com/neuroreport/Abstract/2011/08240/The_effect_of_complement_C5a_on_mitochondrial.4.aspxen_NZ
dc.subjectC5aen_NZ
dc.subjectcentral nervous systemen_NZ
dc.titleThe effect of complement C5a on mitochondrial functions of PC12 cellsen_NZ
dc.typeJournal Articleen_NZ
dc.identifier.doi10.1097/WNR.0b013e32834901d9en_NZ
dc.relation.isPartOfNeuroReporten_NZ
pubs.begin-page581en_NZ
pubs.elements-id36092
pubs.end-page585en_NZ
pubs.issue12en_NZ
pubs.volume22en_NZ


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