Stadlmann 2006 Cell Biochem Biophys: Difference between revisions
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{{Publication | {{Publication | ||
|title=Stadlmann S, Renner K, Pollheimer J, Moser PL, Zeimet AG, Offner FA, Gnaiger E (2006) Preserved coupling of oxydative phosphorylation but decreased mitochondrial respiratory capacity in IL-1Γ treated human peritoneal mesothelial cells. Cell | |title=Stadlmann S, Renner K, Pollheimer J, Moser PL, Zeimet AG, Offner FA, Gnaiger E (2006) Preserved coupling of oxydative phosphorylation but decreased mitochondrial respiratory capacity in IL-1Γ treated human peritoneal mesothelial cells. Cell Biochem Biophys 44: 179-186. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/16456220 PMID: 16456220] | |||
|authors=Stadlmann S, Renner K, Pollheimer J, Moser PL, Zeimet AG, Offner FA, Gnaiger E | |authors=Stadlmann S, Renner K, Pollheimer J, Moser PL, Zeimet AG, Offner FA, Gnaiger E | ||
|year=2006 | |year=2006 | ||
|journal=Cell | |journal=Cell Biochem Biophys | ||
|abstract=The peritoneal mesothelium acts as a regulator of serosal responses to injury, infection, and neoplastic diseases. After inflammation of the serosal surfaces, proinflammatory cytokines induce an βactivatedβ mesothelial cell phenotype, the mitochondrial aspect of which has not previously been studied. After incubation of cultured human peritoneal mesothelial cells with interleukin (IL)-1Ξ² for 48 h, respiratory activity of suspended cells was analyzed by high-resolution respirometry. Citrate synthase (CS) and lactate dehydrogenase (LDH) activities were determined by spectrophotometry. Treatment with IL-1Ξ² resulted in a significant decline of respiratory capacity (''p'' < 0.05). Respiratory control ratios (i.e., uncoupled respiration at optimum carbonyl cyanide p-trifluoromethoxyphenylhydrazone concentration divided by oligomycin inhibited respiration measured in unpermeabilized cells) remained as high as 11, indicating well-coupled mitochondria and functional integrity of the inner mitochondrial membrane. Whereas respiratory capacities of the cells declined in proportion with decreased CS activity (''p'' < 0.05), LDH activity increased (''p'' < 0.05). Taken together, these results indicate that IL-1Ξ² exposure of peritoneal mesothelial cells does not lead to irreversible defects or inhibition of specific components of the respiratory chain, but is associated with a decrease of mitochondrial content of the cells that is correlated with an increase in LDH (and thus glycolytic) capacity. | |abstract=The peritoneal mesothelium acts as a regulator of serosal responses to injury, infection, and neoplastic diseases. After inflammation of the serosal surfaces, proinflammatory cytokines induce an βactivatedβ mesothelial cell phenotype, the mitochondrial aspect of which has not previously been studied. After incubation of cultured human peritoneal mesothelial cells with interleukin (IL)-1Ξ² for 48 h, respiratory activity of suspended cells was analyzed by high-resolution respirometry. Citrate synthase (CS) and lactate dehydrogenase (LDH) activities were determined by spectrophotometry. Treatment with IL-1Ξ² resulted in a significant decline of respiratory capacity (''p'' < 0.05). Respiratory control ratios (i.e., uncoupled respiration at optimum carbonyl cyanide p-trifluoromethoxyphenylhydrazone concentration divided by oligomycin inhibited respiration measured in unpermeabilized cells) remained as high as 11, indicating well-coupled mitochondria and functional integrity of the inner mitochondrial membrane. Whereas respiratory capacities of the cells declined in proportion with decreased CS activity (''p'' < 0.05), LDH activity increased (''p'' < 0.05). Taken together, these results indicate that IL-1Ξ² exposure of peritoneal mesothelial cells does not lead to irreversible defects or inhibition of specific components of the respiratory chain, but is associated with a decrease of mitochondrial content of the cells that is correlated with an increase in LDH (and thus glycolytic) capacity. | ||
|keywords=Peritoneal mesothelial cells, Interleukin-1Ξ², mitochondria, Respiration, Citrate synthase, Lactate dehydrogenase, Cell viability | |keywords=Peritoneal mesothelial cells, Interleukin-1Ξ², mitochondria, Respiration, Citrate synthase, Lactate dehydrogenase, Cell viability | ||
| | |mipnetlab=AT_Innsbruck_Gnaiger E | ||
|discipline=Mitochondrial Physiology, Biomedicine | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
| | |injuries=Mitochondrial Disease; Degenerative Disease and Defect | ||
|organism=Human | |organism=Human | ||
|tissues=Endothelial; Epithelial; Mesothelial Cell | |tissues=Endothelial; Epithelial; Mesothelial Cell | ||
|preparations=Intact Cell; Cultured; Primary | |preparations=Intact Cell; Cultured; Primary | ||
|topics=Respiration; OXPHOS; ETS Capacity, Coupling; Membrane Potential, Mitochondrial Biogenesis; Mitochondrial Density, Substrate; Glucose; TCA Cycle | |topics=Respiration; OXPHOS; ETS Capacity, Coupling; Membrane Potential, Mitochondrial Biogenesis; Mitochondrial Density, Substrate; Glucose; TCA Cycle | ||
|discipline=Mitochondrial Physiology, Biomedicine | |||
}} | }} | ||
Revision as of 20:00, 21 November 2011
| Stadlmann S, Renner K, Pollheimer J, Moser PL, Zeimet AG, Offner FA, Gnaiger E (2006) Preserved coupling of oxydative phosphorylation but decreased mitochondrial respiratory capacity in IL-1Γ treated human peritoneal mesothelial cells. Cell Biochem Biophys 44: 179-186. |
Β» [[Has info::PMID: 16456220]]
Stadlmann S, Renner K, Pollheimer J, Moser PL, Zeimet AG, Offner FA, Gnaiger E (2006) Cell Biochem Biophys
Abstract: The peritoneal mesothelium acts as a regulator of serosal responses to injury, infection, and neoplastic diseases. After inflammation of the serosal surfaces, proinflammatory cytokines induce an βactivatedβ mesothelial cell phenotype, the mitochondrial aspect of which has not previously been studied. After incubation of cultured human peritoneal mesothelial cells with interleukin (IL)-1Ξ² for 48 h, respiratory activity of suspended cells was analyzed by high-resolution respirometry. Citrate synthase (CS) and lactate dehydrogenase (LDH) activities were determined by spectrophotometry. Treatment with IL-1Ξ² resulted in a significant decline of respiratory capacity (p < 0.05). Respiratory control ratios (i.e., uncoupled respiration at optimum carbonyl cyanide p-trifluoromethoxyphenylhydrazone concentration divided by oligomycin inhibited respiration measured in unpermeabilized cells) remained as high as 11, indicating well-coupled mitochondria and functional integrity of the inner mitochondrial membrane. Whereas respiratory capacities of the cells declined in proportion with decreased CS activity (p < 0.05), LDH activity increased (p < 0.05). Taken together, these results indicate that IL-1Ξ² exposure of peritoneal mesothelial cells does not lead to irreversible defects or inhibition of specific components of the respiratory chain, but is associated with a decrease of mitochondrial content of the cells that is correlated with an increase in LDH (and thus glycolytic) capacity. β’ Keywords: Peritoneal mesothelial cells, Interleukin-1Ξ², mitochondria, Respiration, Citrate synthase, Lactate dehydrogenase, Cell viability
β’ O2k-Network Lab: AT_Innsbruck_Gnaiger E
Labels:
Stress:Mitochondrial Disease; Degenerative Disease and Defect Organism: Human Tissue;cell: Endothelial; Epithelial; Mesothelial Cell Preparation: Intact Cell; Cultured; Primary
Regulation: Respiration; OXPHOS; ETS Capacity, Coupling; Membrane Potential, Mitochondrial Biogenesis; Mitochondrial Density, Substrate; Glucose; TCA Cycle
HRR: Oxygraph-2k
