The effect of complement C5a on mitochondrial functions of PC12 cells

R.D. Martinus, C.J. Cook

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

C5a 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. 
Original languageEnglish
Pages (from-to)581-585
Number of pages5
JournalNeuroReport
Volume22
Issue number12
DOIs
Publication statusPublished - 2011
Externally publishedYes

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