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Koziel 2013 Biochem J

From Bioblast
Publications in the MiPMap
Koziel R, Pircher H, Kratochwil M, Lener B, Hermann M, Dencher NA, Jansen-Duerr P (2013) Mitochondrial respiratory chain complex I is inactivated by NADPH oxidase Nox4. Biochem J 452:231-9.

ยป PMID: 23514110 Open Access

Koziel R, Pircher H, Kratochwil M, Lener B, Hermann M, Dencher NA, Jansen-Duerr P (2013) Biochem J

Abstract: ROS (reactive oxygen species) generated by NADPH oxidases play an important role in cellular signal transduction regulating cell proliferation, survival and differentiation. Nox4 (NADPH oxidase 4) induces cellular senescence in human endothelial cells; however, intracellular targets for Nox4 remained elusive. In the present study, we show that Nox4 induces mitochondrial dysfunction in human endothelial cells. Nox4 depletion induced alterations in mitochondrial morphology, stabilized mitochondrial membrane potential and decreased production of H2O2 in mitochondria. High-resolution respirometry in permeabilized cells combined with native PAGE demonstrated that Nox4 specifically inhibits the activity of mitochondrial electron transport chain complex I, and this was associated with a decreased concentration of complex I subunits. These data suggest a new pathway by which sustained Nox4 activity decreases mitochondrial function. โ€ข Keywords: Complex I, Eelectron transport chain, Mitochondrion, Nox4, Oxidative stress, Senescence

โ€ข O2k-Network Lab: AT Innsbruck Jansen-Duerr P


Labels: MiParea: Respiration  Pathology: Aging;senescence 

Organism: Human  Tissue;cell: Endothelial;epithelial;mesothelial cell  Preparation: Permeabilized cells 


Coupling state: OXPHOS 

HRR: Oxygraph-2k