The effect of complement C5a on mitochondrial functions of PC12 cells

R.D. Martinus, C.J. Cook

Research output: Contribution to journalArticle

2 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

Fingerprint

Complement C5a
PC12 Cells
Mitochondria
Chaperonin 60
Mitochondrial Proteins
Electron Transport Complex IV
Heat-Shock Proteins
Cultured Cells
Oxidoreductases
Respiration
Cell Death
Central Nervous System
Apoptosis

Cite this

Martinus, R.D. ; Cook, C.J. / The effect of complement C5a on mitochondrial functions of PC12 cells. In: NeuroReport. 2011 ; Vol. 22, No. 12. pp. 581-585.
@article{b8985b6b9aa841008a7c3af8f5d8e2f1,
title = "The effect of complement C5a on mitochondrial functions of PC12 cells",
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. ",
keywords = "C5a, chaperonin 60, complement, mitochondria, neuronal",
author = "R.D. Martinus and C.J. Cook",
note = "Cited By :2 Export Date: 25 May 2017",
year = "2011",
doi = "10.1097/WNR.0b013e32834901d9",
language = "English",
volume = "22",
pages = "581--585",
journal = "NeuroReport",
issn = "0959-4965",
publisher = "Lippincott Williams and Wilkins",
number = "12",

}

The effect of complement C5a on mitochondrial functions of PC12 cells. / Martinus, R.D.; Cook, C.J.

In: NeuroReport, Vol. 22, No. 12, 2011, p. 581-585.

Research output: Contribution to journalArticle

TY - JOUR

T1 - The effect of complement C5a on mitochondrial functions of PC12 cells

AU - Martinus, R.D.

AU - Cook, C.J.

N1 - Cited By :2 Export Date: 25 May 2017

PY - 2011

Y1 - 2011

N2 - 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. 

AB - 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. 

KW - C5a

KW - chaperonin 60

KW - complement

KW - mitochondria

KW - neuronal

U2 - 10.1097/WNR.0b013e32834901d9

DO - 10.1097/WNR.0b013e32834901d9

M3 - Article

VL - 22

SP - 581

EP - 585

JO - NeuroReport

JF - NeuroReport

SN - 0959-4965

IS - 12

ER -