Difference between revisions of "Lemieux 2019 bioRxiv"
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== Preprints for Gentle Science == | |||
::::» [[Gentle_Science#Preprints_for_Gentle_Science |Preprints for Gentle Science]] | |||
[[Image:MITOEAGLE-logo.jpg|60px|link=http://www.mitoglobal.org/index.php/MitoEAGLE|COST Action MitoEAGLE]] In the spirit of COST Action [[WG1_MitoEAGLE_protocols,_terminology,_documentation#Documentation |MitoEAGLE WG1]] | |||
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Revision as of 08:41, 13 January 2021
| Lemieux H, Subarsky P, Doblander C, Wurm M, Troppmair J, Gnaiger E (2019) Mitochondrial respiratory function as an early biomarker of apoptosis induced by growth factor removal. bioRxiv doi: https://doi.org/10.1101/151480 . |
» Version 2 (2019-06-11) in preparation, bioRxiv Preprint Version 1 Open Access
Lemieux H, Subarsky P, Doblander C, Wurm M, Troppmair J, Gnaiger E (2019) bioRxiv
Abstract: Remodeling of mitochondrial metabolism is implicated in progression of cancer. Conversely, however, mitochondrial dysfunction and signaling play key roles in the induction of cell death. Apoptosis is induced following interleukin 3 (IL-3) depletion in mouse pro-myeloid 32D cells. Molecular signals of cell death are absent in 32D cells after short-term IL-3 deprivation (8 h). We addressed the question if changes in mitochondrial function can be detected by high-resolution respirometry as an early event in the induction of apoptosis. Respiration of living 32D cells was suppressed by 10 to 55% following 8 h removal of IL-3, but remained more stable in 32D cells expressing the v-RAF oncogene related to CRAF. In 32D cells deprived of IL3, succinate-supported respiration did not decline significantly, but respiratory capacities of the NADH-pathway and the combined NADH- and succinate-linked (NS) pathway were decreased compared to cells grown in the presence of IL-3. This was consistent with respiratory control exerted by impaired Complex IV activity, since there was not even the slightest excess Complex IV capacity above NS-pathway capacity. In contrast, electron flow reached only 60% when supported by succinate alone through Complexes II, III and IV, and was therefore relatively insensitive to Complex IV injuries up to a threshold of 40% inhibition. After IL-3 depletion respiration increased by 15% following addition of cytochrome c, which provides a marker of mitochondrial outer membrane leakage, thus indicating mitochondrial fragility. Our results highlight a novel link between the key mitogenic and survival kinase CRAF and mitochondrial energy homeostasis. • Keywords: Mitochondrial respiration, OXPHOS, cytochrome c oxidase, apoptosis, CRAF, interleukin 3 • Bioblast editor: Gnaiger E • O2k-Network Lab: CA_Edmonton_Lemieux H, AT_Innsbruck_Oroboros, AT_Innsbruck_Gnaiger E
Preprints for Gentle Science
In the spirit of COST Action MitoEAGLE WG1
Contribution to K-Regio MitoFit
Template:Cited in Gnaiger 2000 BEC MitoPathways
Labels: MiParea: Respiration Pathology: Cancer Stress:Cell death Organism: Mouse Tissue;cell: Blood cells Preparation: Intact cells, Permeabilized cells Enzyme: Complex IV;cytochrome c oxidase, Marker enzyme Regulation: Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, Threshold;excess capacity, Uncoupler, Q-junction effect Coupling state: LEAK, ROUTINE, OXPHOS, ET Pathway: N, S, CIV, NS, ROX HRR: Oxygraph-2k
MitoEAGLEPublication, BEC 2020.2
