Koziel 2012 Abstract Bioblast

From Bioblast
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

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.

  1. 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. 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

β€’ Keywords: Mitochondria, HUVEC, Senescence, Reactive oxygen species

β€’ 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: [email protected]

(2) Technische UniversitΓ€t 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


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