The effect of complement C5a on mitochondrial functions of PC12 cells

Reference:

Martinus, R. D. and Cook, C. J., 2011. The effect of complement C5a on mitochondrial functions of PC12 cells. Neuroreport, 22 (12), pp. 581-585.

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Official URL:

http://dx.doi.org/10.1097/WNR.0b013e32834901d9

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.

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