Stadlmann 2006 Cell Biochem Biophys

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-1ß treated human peritoneal mesothelial cells. Cell Biochem Biophys 44:179-86.

» 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 “activated” mesothelial cell phenotype, the mitochondrial aspect of which has not previously been studied. After incubation of cultured human peritoneal mesothelial cells with interleukin (IL)-1β 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-1β 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-1β 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-1β, Mitochondria, Respiration, Citrate synthase, Lactate dehydrogenase, Cell viability

• O2k-Network Lab: AT Innsbruck Gnaiger E

Labels: MiParea: Respiration, mt-Biogenesis;mt-density, Pharmacology;toxicology 

Stress:Cell death  Organism: Human  Tissue;cell: Endothelial;epithelial;mesothelial cell  Preparation: Intact cells 

Regulation: Coupling efficiency;uncoupling, Substrate  Coupling state: ROUTINE, ETS"ETS" is not in the list (LEAK, ROUTINE, OXPHOS, ET) of allowed values for the "Coupling states" property. 

HRR: Oxygraph-2k 

Coupling control protocol

» CCP Stadlmann 2006 Cell Biochem Biophys

Step	<Symbol in 2006 publication>	Respiratory state	Pathway control	Comment
R	< E >	ROUTINE	ce	pce without substrate are in a state of ROX.
1SD	< S >	R&SP	ROUTINE & S (R&P)	pce are in state SP.
2Omy	< O >	R&SL	ROUTINE & S (L)	ce and pce are in the LEAK state.
3U	< 3u >	E&SE	ETS & S (E)	ce and pce are in the ETS state.
4Rot	< R >	SE	ROX & S (E)	ce are in the ROX state, pce are in the ETS state.
5Ama	< A >	ROXAma	ROX