0000000000643209

AUTHOR

Annika Pfeiffer

showing 3 related works from this author

Mitochondrial function and energy metabolism in neuronal HT22 cells resistant to oxidative stress

2014

Background and Purpose The hippocampal cell line HT22 is an excellent model for studying the consequences of endogenous oxidative stress. Extracellular glutamate depletes cellular glutathione by blocking the glutamate/cystine antiporter system xc−. Glutathione depletion induces a well-defined programme of cell death characterized by an increase in reactive oxygen species and mitochondrial dysfunction. Experimental Approach We compared the mitochondrial shape, the abundance of mitochondrial complexes and the mitochondrial respiration of HT22 cells, selected based on their resistance to glutamate, with those of the glutamate-sensitive parental cell line. Key Results Glutamate-resistant mitoch…

PharmacologyOligomycinATP synthaseCellular respirationOxidative phosphorylationMitochondrionBiologymedicine.disease_causechemistry.chemical_compoundMitochondrial permeability transition poreBiochemistrychemistrymedicinebiology.proteinATP–ADP translocaseOxidative stressBritish Journal of Pharmacology
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Stromal Interaction Molecule 1 (STIM1) Is Involved in the Regulation of Mitochondrial Shape and Bioenergetics and Plays a Role in Oxidative Stress

2012

Calcium ions are involved in a plethora of cellular functions including cell death and mitochondrial energy metabolism. Store-operated Ca(2+) entry over the plasma membrane is activated by depletion of intracellular Ca(2+) stores and is mediated by the sensor STIM1 and the channel ORAI1. We compared cell death susceptibility to oxidative stress in STIM1 knock-out and ORAI1 knockdown mouse embryonic fibroblasts and in knock-out cells with reconstituted wild type and dominant active STIM1. We show that STIM1 and ORAI1 deficiency renders cells more susceptible to oxidative stress, which can be rescued by STIM1 and ORAI1 overexpression. STIM1 knock-out mitochondria are tubular, have a higher Ca…

inorganic chemicalsProgrammed cell deathORAI1 ProteinEukaryotic Initiation Factor-2Active Transport Cell NucleusApoptosisMitochondrionBiologymedicine.disease_causeBiochemistryMiceeIF-2 KinasemedicineAnimalsStromal Interaction Molecule 1PhosphorylationMolecular BiologyTranscription factorCells CulturedMice KnockoutEIF-2 kinaseMembrane GlycoproteinsEndoplasmic reticulumMolecular Bases of DiseaseSTIM1Cell BiologyFibroblastsEmbryo MammalianMitochondriaCell biologyOxidative Stressbiology.proteinCalciumCalcium ChannelsEnergy MetabolismIntracellularOxidative stressJournal of Biological Chemistry
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Bcl-xL knockout attenuates mitochondrial respiration and causes oxidative stress that is compensated by pentose phosphate pathway activity

2017

Bcl-xL is an anti-apoptotic protein that localizes to the outer mitochondrial membrane and influences mitochondrial bioenergetics by controlling Ca2+ influx into mitochondria. Here, we analyzed the effect of mitochondrial Bcl-xL on mitochondrial shape and function in knockout (KO), wild type and rescued mouse embryonic fibroblast cell lines. Mitochondria of KO cells were more fragmented, exhibited a reduced ATP concentration, and reduced oxidative phosphorylation (OXPHOS) suggesting an increased importance of ATP generation by other means. Under steady-state conditions, acidification of the growth medium as a readout for glycolysis was similar, but upon inhibition of ATP synthase with oligo…

0301 basic medicineOligomycinBioenergeticsOxidative phosphorylationBH4 DOMAINMitochondrionPentose phosphate pathwaymedicine.disease_causeBiochemistryCYTOCHROME-C03 medical and health scienceschemistry.chemical_compoundCHANNEL VDAC0302 clinical medicinePhysiology (medical)BCL-XLmedicineJournal ArticleGlycolysisRELEASEATP synthasebiologyGLUCOSE-METABOLISMFISSIONAPOPTOSIS030104 developmental biologyBiochemistrychemistryCELLSbiology.proteinMEMBRANE030217 neurology & neurosurgeryOxidative stressFree Radical Biology and Medicine
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