原创力文档uncoupling protein-4 (ucp4) increases atp supply by interacting with mitochondrial complex ii in neuroblastoma cells解偶联含有(ucp4)增加atp供应与线粒体交互复杂二世在神经母细胞瘤细胞.pdfVIP
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uncoupling protein-4 (ucp4) increases atp supply by interacting with mitochondrial complex ii in neuroblastoma cells解偶联含有(ucp4)增加atp供应与线粒体交互复杂二世在神经母细胞瘤细胞
Uncoupling Protein-4 (UCP4) Increases ATP Supply by
Interacting with Mitochondrial Complex II in
Neuroblastoma Cells
1,3 1,3 1 1 1
Philip Wing-Lok Ho *, Jessica Wing-Man Ho , Ho-Man Tse , Danny Hon-Fai So , David Chi-Wai Yiu ,
1 1,3 1 2 1,3
Hui-Fang Liu , Koon-Ho Chan , Michelle Hiu-Wai Kung , David Boyer Ramsden , Shu-Leong Ho
1 Division of Neurology, University Department of Medicine, University of Hong Kong, Hong Kong, Hong Kong, 2 School of Medicine and School of Biosciences, University
of Birmingham, Birmingham, United Kingdom, 3 Research Centre of Heart, Brain, Hormone and Healthy Aging (HBHA), University of Hong Kong, Hong Kong, Hong Kong
Abstract
Mitochondrial uncoupling protein-4 (UCP4) protects against Complex I deficiency as induced by 1-methyl-4-
phenylpyridinium (MPP+), but how UCP4 affects mitochondrial function is unclear. Here we investigated how UCP4 affects
mitochondrial bioenergetics in SH-SY5Y cells. Cells stably overexpressing UCP4 exhibited higher oxygen consumption
(10.1%, p,0.01), with 20% greater proton leak than vector controls (p,0.01). Increased ATP supply was observed in UCP4-
overexpressing cells compared to controls (p,0.05). Although state 4 and state 3 respiration rates of UCP4-overexpressing
and control cells were similar, Complex II activity in UCP4-overexpressing cells was 30% higher (p,0.05), associated with
protein binding between UCP4 and Complex II, but not that of either Complex I or IV. Mitochondrial ADP consumption by
succinate-induced respiration was 26% higher in UCP4-overe
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