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See detailEvidence of oxidative stress and mitochondrial respiratory chain dysfunction in an in vitro model of sepsis-induced kidney injury
Quoilin, Caroline ULg; Mouithys-Mickalad, Ange ULg; Lécart, Sandrine et al

in Biochimica et Biophysica Acta-Bioenergetics (2014), 1837(10), 1790-1800

To investigate the role of oxidative stress and/or mitochondrial impairment in the occurrence of acute kidney injury (AKI) during sepsis, we developed a sepsis-induced in vitro model using proximal ... [more ▼]

To investigate the role of oxidative stress and/or mitochondrial impairment in the occurrence of acute kidney injury (AKI) during sepsis, we developed a sepsis-induced in vitro model using proximal tubular epithelial cells exposed to a bacterial endotoxin (lipopolysaccharide, LPS). This investigation has provided key features on the relationship between oxidative stress and mitochondrial respiratory chain activity defects. LPS treatment resulted in an increase in the expression of inducible nitric oxide synthase (iNOS) and NADPH oxidase 4 (NOX-4), suggesting the cytosolic overexpression of nitric oxide and superoxide anion, the primary reactive nitrogen species (RNS) and reactive oxygen species (ROS). This oxidant state seemed to interrupt mitochondrial oxidative phosphorylation by reducing cytochrome c oxidase activity. As a consequence, disruptions in the electron transport and the proton pumping across the mitochondrial inner membrane occurred, leading to a decrease of the mitochondrial membrane potential, a release of apoptotic-inducing factors and a depletion of adenosine triphosphate. Interestingly, after being targeted by RNS and ROS, mitochondria became in turn producer of ROS, thus contributing to increase the mitochondrial dysfunction. The role of oxidants in mitochondrial dysfunction was further confirmed by the use of iNOS inhibitors or antioxidants that preserve cytochrome c oxidase activity and prevent mitochondrial membrane potential dissipation. These results suggest that sepsis-induced AKI should not only be regarded as failure of energy status but also as an integrated response, including transcriptional events, ROS signaling, mitochondrial activity and metabolic orientation such as apoptosis. [less ▲]

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See detailDisruption in energy metabolism and mitochondrial function in a cellular model of inflammation-induced acute kidney injury
Quoilin, Caroline ULg; Mouithys-Mickalad, Ange ULg; Lécart, Sandrine et al

Poster (2013, September)

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 ... [more ▼]

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. [less ▲]

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See detailAn ESR, Mass Spectrometry and Fluorescence microscopy approach to study the stearic acid derivatives anchoring in cells
Grammenos, Angeliki ULg; Fillet, Marianne ULg; Collodoro, Mike et al

in Applied Magnetic Resonance (2012)

Lateral phase separations in biological membranes are of great interest, making Electron Spin Resonance (ESR) spectroscopy combined with spin labelling a non destructive and sensitive technique for the ... [more ▼]

Lateral phase separations in biological membranes are of great interest, making Electron Spin Resonance (ESR) spectroscopy combined with spin labelling a non destructive and sensitive technique for the study of lipid rafts. This is currently accepted that spin probe localization is on the plasma membrane. However, no study confirms this hypothesis. Herein, we report, for the first time, an accurate multi spectral method for the quantification of lipid spin label presence in every sub-cellular fraction. Cells were incubated with 5-doxyl stearic acid derivative and then sub-fractionated. Results of our multimodal spectroscopy approach ubiquitously demonstrate that the presence of ESR spin label only sets in the plasma membranes. [less ▲]

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