Hernandez-Alvarez 2013 Antioxid Redox Signal: Difference between revisions
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{{Publication | {{Publication | ||
|title=Hernández-Alvarez MI, Paz JC, Sebastián D, Muñoz JP, Liesa M, Segalés J, Palacín M, Zorzano A (2013) Glucocorticoid modulation of mitochondrial function in hepatoma cells requires the mitochondrial fission protein Drp1. Antioxid Redox Signal 19: 366-378. | |title=Hernández-Alvarez MI, Paz JC, Sebastián D, Muñoz JP, Liesa M, Segalés J, Palacín M, Zorzano A (2013) Glucocorticoid modulation of mitochondrial function in hepatoma cells requires the mitochondrial fission protein Drp1. Antioxid Redox Signal 19: 366-378. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/22703557 PMID:22703557] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/22703557 PMID:22703557] | ||
|authors=Hernández-Alvarez MI, Paz JC, Sebastián D, Muñoz JP, Liesa M, Segalés J, Palacín M, Zorzano A | |authors=Hernández-Alvarez MI, Paz JC, Sebastián D, Muñoz JP, Liesa M, Segalés J, Palacín M, Zorzano A | ||
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CONCLUSION: | CONCLUSION: | ||
In summary, we demonstrate that the mitochondrial effects of dexamethasone both on mitochondrial respiration and on the gluconeogenic pathway depend on Drp1. | In summary, we demonstrate that the mitochondrial effects of dexamethasone both on mitochondrial respiration and on the gluconeogenic pathway depend on Drp1. | ||
|keywords=mitochondrial dynamics, dexasmethason, gluconeogenesis, mitofusin | |||
|mipnetlab=ES Barcelona Zorzano A | |mipnetlab=ES Barcelona Zorzano A | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration | |area=Respiration, mt-Structure;fission;fusion, Genetic knockout;overexpression | ||
|organism=Rat | |||
|tissues=Liver | |||
|model cell lines=Other cell lines | |||
|preparations=Homogenate | |||
|injuries=RONS; Oxidative Stress | |||
|couplingstates=OXPHOS, ETS | |||
|substratestates=CI, CII, CI+II, ROX | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} |
Revision as of 12:05, 7 October 2013
Hernández-Alvarez MI, Paz JC, Sebastián D, Muñoz JP, Liesa M, Segalés J, Palacín M, Zorzano A (2013) Glucocorticoid modulation of mitochondrial function in hepatoma cells requires the mitochondrial fission protein Drp1. Antioxid Redox Signal 19: 366-378. |
Hernández-Alvarez MI, Paz JC, Sebastián D, Muñoz JP, Liesa M, Segalés J, Palacín M, Zorzano A (2013) Antioxid Redox Signal
Abstract: AIMS: Glucocorticoids, such as dexamethasone, enhance hepatic energy metabolism and gluconeogenesis partly through changes in mitochondrial function. Mitochondrial function is influenced by the balance between mitochondrial fusion and fission events. However, whether glucocorticoids modulate mitochondrial function through the regulation of mitochondrial dynamics is currently unknown.
RESULTS: Here, we report that the effects of dexamethasone on mitochondrial function and gluconeogenesis in hepatoma cells are dependent on the mitochondrial fission protein dynamin-related protein 1 (Drp1). Dexamethasone increased routine oxygen consumption, maximal respiratory capacity, superoxide anion, proton leak, and gluconeogenesis in hepatoma cells. Under these conditions, dexamethasone altered mitochondrial morphology, which was paralleled by a large increase in Drp1 expression, and reduced mitofusin 1 (Mfn1) and Mfn2. In vivo dexamethasone treatment also enhanced Drp1 expression in mouse liver. On the basis of these observations, we analyzed the dependence on the Drp1 function of dexamethasone effects on mitochondrial respiration and gluconeogenesis. We show that the increase in mitochondrial respiration and gluconeogenesis induced by dexamethasone are hampered by the inhibition of Drp1 function.
INNOVATION: Our findings provide the first evidence that the effects of glucocorticoids on hepatic metabolism require the mitochondrial fission protein Drp1.
CONCLUSION: In summary, we demonstrate that the mitochondrial effects of dexamethasone both on mitochondrial respiration and on the gluconeogenic pathway depend on Drp1. • Keywords: mitochondrial dynamics, dexasmethason, gluconeogenesis, mitofusin
• O2k-Network Lab: ES Barcelona Zorzano A
Labels: MiParea: Respiration, mt-Structure;fission;fusion, Genetic knockout;overexpression
Stress:RONS; Oxidative Stress"RONS; Oxidative Stress" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. Organism: Rat Tissue;cell: Liver Preparation: Homogenate
Coupling state: OXPHOS, ETS"ETS" is not in the list (LEAK, ROUTINE, OXPHOS, ET) of allowed values for the "Coupling states" property.
HRR: Oxygraph-2k