期刊
NEUROREPORT
卷 22, 期 12, 页码 581-585出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/WNR.0b013e32834901d9
关键词
C5a; chaperonin 60; complement; mitochondria; neuronal
资金
- Foundation for Research Science and Technology of New Zealand
- EPSRC [EP/H009744/1] Funding Source: UKRI
- Engineering and Physical Sciences Research Council [EP/H009744/1] Funding Source: researchfish
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. NeuroReport 22:581-585 (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
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