Poster (Scientific congresses and symposiums)
Disruption in energy metabolism and mitochondrial function in a cellular model of inflammation-induced acute kidney injury
Quoilin, Caroline; Mouithys-Mickalad, Ange; Lécart, Sandrine et al.
2013SFRR-Europe 2013 Conference
 

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Keywords :
Sepsis; Acute Kidney Injury; Mitochondrial dysfunction; Respiratory Chain; Cytopathic hypoxia
Abstract :
[en] Sepsis is a very complex clinical condition characterized by stimulation of a systemic inflammatory response due to an infection. It has a profound deleterious effect on kidney functions leading to sepsis-induced acute kidney injury (AKI). This failure seems to occur through complex mechanisms involving the immune system response, inflammatory pathways, cellular dysfunction and hemodynamic instability. To study the role of cellular energetic metabolism dysfunction and mitochondrial impairment in the occurrence of AKI during sepsis, we developed an inflammation-induced in vitro model using proximal tubular epithelial cells (HK-2) exposed to a bacterial endotoxin (lipopolysaccharide, LPS). This investigation has provided key features on the relationship between endotoxic stress and mitochondrial respiratory chain assembly defects. Firstly, we have shown that renal cells subjected to LPS are no longer capable to use adequately the available oxygen to maintain their metabolic functions. One hypothesis of this down-regulation suggests that impairment in mitochondria oxidative phosphorylation could prevent cells from using oxygen for adenosine triphosphate (ATP) production and potentially could cause sepsis-induced organ failure. Our study has then investigated this possible mitochondrial impairment to explain the decreased O2 consumption rate observed in LPS-treated HK-2 cells. After exposure to LPS, functionality of mitochondria was affected without any disturbance in their spatial organization. LPS seemed rather to interrupt mitochondrial oxidative phosphorylation by blocking cytochrome c oxidase activity. As a consequence, disruptions in the electron transport and the proton pumping across the system occurred, leading to a decrease of the mitochondrial membrane potential, an electron leakage as the form of superoxide anion, a release of cytochrome c in the cytosol and a decrease in ATP production. This irreversible defect in the production of cellular energy would support the concept that kidney failure in sepsis may occur on the basis of cytopathic hypoxia.
Research center :
Laboratoire de Spectroscopie Biomédicale
Disciplines :
Physical, chemical, mathematical & earth Sciences: Multidisciplinary, general & others
Biochemistry, biophysics & molecular biology
Author, co-author :
Quoilin, Caroline ;  Université de Liège - ULiège > Département de physique > Spectroscopie biomédicale
Mouithys-Mickalad, Ange ;  Université de Liège - ULiège > Centre de l'oxygène : Recherche et développement (C.O.R.D.)
Lécart, Sandrine
Gallez, Bernard
Fontaine-Aupart, Marie-Pierre
Hoebeke, Maryse  ;  Université de Liège - ULiège > Département de physique > Spectroscopie biomédicale
Language :
English
Title :
Disruption in energy metabolism and mitochondrial function in a cellular model of inflammation-induced acute kidney injury
Publication date :
September 2013
Event name :
SFRR-Europe 2013 Conference
Event place :
Athens, Greece
Event date :
du 23 au 25 septembre 2013
Audience :
International
Funders :
F.R.S.-FNRS - Fonds de la Recherche Scientifique [BE]
ULiège - Université de Liège [BE]
Available on ORBi :
since 02 October 2013

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