Difference between revisions of "Koziel 2012 Abstract Bioblast"
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{{Abstract | {{Abstract | ||
|title=Koziel R, Pircher H, Kratochwil M, Lener B, Hermann M, Dencher N.A, Jansen-Durr P (2012) | |title=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. | ||
|info=[[MiPNet17.12 Bioblast 2012|MiPNet17.12 Bioblast 2012 - Open Access]] | |info=[[MiPNet17.12 Bioblast 2012|MiPNet17.12 Bioblast 2012 - Open Access]] | ||
|authors=Koziel R, Pircher H, Kratochwil M, Lener B, Hermann M, Dencher NA, Jansen- | |authors=Koziel R, Pircher H, Kratochwil M, Lener B, Hermann M, Dencher NA, Jansen-Duerr P | ||
|year=2012 | |year=2012 | ||
|event=[[Bioblast 2012]] | |event=[[Bioblast 2012]] | ||
|abstract=Oxygen radicals produced by NADPH oxidases play an important role in regulating cell proliferation, survival and differentiation. NADPH oxidase 4 (Nox4) induces cellular senescence in human endothelial cells; 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. | |abstract=[[File:R Koziel small.jpg|right|150px|Rafal Koziel]] | ||
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. | |||
# [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] | |||
# [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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}} | }} | ||
{{Labeling | {{Labeling | ||
|diseases=Aging;senescence | |||
|injuries=Oxidative stress;RONS | |||
|tissues=HUVEC | |||
|preparations=Intact cells, Permeabilized cells, Isolated mitochondria | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|journal=Mitochondr Physiol Network | |journal=Mitochondr Physiol Network | ||
|articletype=Abstract | |articletype=Abstract | ||
| Line 25: | Line 29: | ||
== Affiliations and author contributions == | == Affiliations and author contributions == | ||
Institute for Biomedical Aging Research, University | 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: Rafal.Koziel@uibk.ac.at | |||
(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 | |||
== Help == | == Help == | ||
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Latest revision as of 15:58, 9 November 2016
| 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-Duerr 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.
- 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
- 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
• O2k-Network Lab: AT Innsbruck Jansen-Duerr P
Labels: Pathology: Aging;senescence Stress:Oxidative stress;RONS
Tissue;cell: HUVEC Preparation: Intact cells, Permeabilized cells, Isolated mitochondria
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: Rafal.Koziel@uibk.ac.at
(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
