Difference between revisions of "Koziel 2012 Abstract Bioblast"
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Oxygen radicals produced by NADPH oxidases play an important role in regulating cell proliferation, survival and differentiation [1]. NADPH oxidase 4 (Nox4) induces cellular senescence in human endothelial cells [2]; however mechanisms of senescence induction remained elusive. Here we show that Nox4 induces mitochondrial dysfunction in human endothelial cells. Nox4 depletion induced alterations in mitochondrial morphology, stabilized mitochondrial membrane potential, and decreased mitochondrial production of free radicals. Importantly, respiratory activity decreased with extended passaging in control cells but was maintained at high level in Nox4-depleted cells, suggesting that mitochondrial energy production is compromised by Nox4. | Oxygen radicals produced by NADPH oxidases play an important role in regulating cell proliferation, survival and differentiation [1]. NADPH oxidase 4 (Nox4) induces cellular senescence in human endothelial cells [2]; however mechanisms of senescence induction remained elusive. Here we show that Nox4 induces mitochondrial dysfunction in human endothelial cells. Nox4 depletion induced alterations in mitochondrial morphology, stabilized mitochondrial membrane potential, and decreased mitochondrial production of free radicals. Importantly, respiratory activity decreased with extended passaging in control cells but was maintained at high level in Nox4-depleted cells, suggesting that mitochondrial energy production is compromised by Nox4. | ||
[1] [http://www.ncbi.nlm.nih.gov/pubmed/21273445 Sampson N, Koziel R, Zenzmaier C, Bubendorf L, Plas E, Jansen-Duerr P, Berger P ROS signaling by NOX4 drives fibroblast-to-myofibroblast differentiation in the diseased prostatic stroma. Mol Endocrinol. 25: 503-515 Open Access] | |||
[2] [http://www.ncbi.nlm.nih.gov/pubmed/19681754 Lener B, Koziel R, Pircher H, Huetter E, Greussing R, Herndler-Brandstetter D, Hermann M, Unterluggauer H, Jansen-Duerr P (2009) The NADPH oxidase Nox4 restricts the replicative lifespan of human endothelial cells. Biochem J 423: 363-374 Open Access] | |||
|keywords=Mitochondria, HUVEC, Senescence, Reactive oxygen species | |keywords=Mitochondria, HUVEC, Senescence, Reactive oxygen species | ||
|mipnetlab=AT Innsbruck Jansen-Duerr P | |mipnetlab=AT Innsbruck Jansen-Duerr P | ||
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Koziel R (1), Pircher H (1), Kratochwil M (4), Lener B (1,2), Hermann M (3), Dencher NA (4), Jansen-Durr P (1,2) | Koziel R (1), Pircher H (1), Kratochwil M (4), Lener B (1,2), Hermann M (3), Dencher NA (4), Jansen-Durr P (1,2) | ||
(1) Institute for Biomedical Aging Research, Innsbruck University, Innsbruck, Austria; Email: | (1) Institute for Biomedical Aging Research, Innsbruck University, Innsbruck, Austria; Email: Rafal.Koziel@uibk.ac.at | ||
(2) Technische Universität Darmstadt, Department of Chemistry, Physical Biochemistry, Darmstadt, Germany | (2) Technische Universität Darmstadt, Department of Chemistry, Physical Biochemistry, Darmstadt, Germany | ||
Revision as of 15:02, 22 November 2012
| Koziel R, Pircher H, Kratochwil M, Lener B, Hermann M, Dencher N.A, Jansen-Durr P (2012) NADPH oxidase Nox4 induces mitochondrial dysfunction in human endothelial cells. Mitochondr Physiol Network 17.12. |
Link: MiPNet17.12 Bioblast 2012 - Open Access
Koziel R, Pircher H, Kratochwil M, Lener B, Hermann M, Dencher NA, Jansen-Durr P (2012)
Event: Bioblast 2012
Oxygen radicals produced by NADPH oxidases play an important role in regulating cell proliferation, survival and differentiation [1]. NADPH oxidase 4 (Nox4) induces cellular senescence in human endothelial cells [2]; however mechanisms of senescence induction remained elusive. Here we show that Nox4 induces mitochondrial dysfunction in human endothelial cells. Nox4 depletion induced alterations in mitochondrial morphology, stabilized mitochondrial membrane potential, and decreased mitochondrial production of free radicals. Importantly, respiratory activity decreased with extended passaging in control cells but was maintained at high level in Nox4-depleted cells, suggesting that mitochondrial energy production is compromised by Nox4.
• Keywords: Mitochondria, HUVEC, Senescence, Reactive oxygen species
• O2k-Network Lab: AT Innsbruck Jansen-Duerr P
Labels:
Stress:RONS; Oxidative Stress"RONS; Oxidative Stress" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property., Aging; Senescence"Aging; Senescence" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. Organism: Human Tissue;cell: Endothelial; Epithelial; Mesothelial Cell"Endothelial; Epithelial; Mesothelial Cell" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property. Preparation: Intact Cell; Cultured; Primary"Intact Cell; Cultured; Primary" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property., Permeabilized cells, Isolated Mitochondria"Isolated Mitochondria" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property.
HRR: Oxygraph-2k
Affiliations and author contributions
Koziel R (1), Pircher H (1), Kratochwil M (4), Lener B (1,2), Hermann M (3), Dencher NA (4), Jansen-Durr P (1,2)
(1) Institute for Biomedical Aging Research, Innsbruck University, Innsbruck, Austria; Email: [email protected]
(2) Technische Universität Darmstadt, Department of Chemistry, Physical Biochemistry, Darmstadt, Germany
(3) Tiroler Krebsforschungsinstitut, Innsbruck, Austria
(4) KMT Laboratory, Department of Visceral, Transplant and Thoracic Surgery, Center for Operative Medicine, Innsbruck, Austria
