CELLULAR, MOLECULAR AND DEVELOPMENTAL NEUROSCIENCEThe effect of complement C5a on mitochondrial functions of PC12 cellsMartinus, Ryan D.a,b; Cook, Christian J.a,c,d Author Information aHortResearch, Ruakura Research Centre, Hamilton, New Zealand bDepartment of Biological Sciences, Faculty of Science and Engineering, The University of Waikato, Hamilton, New Zealand cHamlyn Centre, Imperial College, London dDepartment for Health, University of Bath, Bath, UK Correspondence to Ryan D. Martinus, Department of Biological Sciences, Faculty of Science and Engineering, University of Waikato, Private Bag 3105, Hamilton, New Zealand Tel: +64 07 8384375; fax: +64 07 8384324; e-mail: [email protected] Received March 23, 2011 Accepted May 19, 2011 NeuroReport: August 24, 2011 - Volume 22 - Issue 12 - p 581-585 doi: 10.1097/WNR.0b013e32834901d9 Buy Metrics 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. © 2011 Lippincott Williams & Wilkins, Inc.