Difference between revisions of "Djafarzadeh 2011 Mitochondrion"
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{{Publication | {{Publication | ||
|title=Djafarzadeh S, Vuda M, Takala J, Ochs M, Jakob SM (2011) Toll-like receptor-3-induced mitochondrial dysfunction in cultured human hepatocytes. Mitochondrion 11 | |title=Djafarzadeh S, Vuda M, Takala J, Ochs M, Jakob SM (2011) Toll-like receptor-3-induced mitochondrial dysfunction in cultured human hepatocytes. Mitochondrion 11:83-8. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/20691286] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/20691286 PMID: 20691286] | ||
|authors=Djafarzadeh S, Vuda M, Takala J, Ochs M, Jakob SM | |authors=Djafarzadeh S, Vuda M, Takala J, Ochs M, Jakob SM | ||
|year=2011 | |year=2011 | ||
|journal=Mitochondrion | |journal=Mitochondrion | ||
|abstract=Several studies have shown the presence of liver mitochondrial dysfunction during | |abstract=Several studies have shown the presence of liver mitochondrial dysfunction during sepsis. TLR3 recognizes viral double-stranded RNA and host endogenous cellular mRNA released from damaged cells. TLR3 ligand amplifies the systemic | ||
sepsis. TLR3 recognizes viral double-stranded RNA and host endogenous cellular | hyperinflammatory response observed during sepsis and in sepsis RNA escaping from damaged tissues/cells may serve as an endogenous ligand for TLR3 thereby | ||
mRNA released from damaged cells. TLR3 ligand amplifies the systemic | modulating immune responses. This study addressed the hypothesis that TLR3 might | ||
hyperinflammatory response observed during sepsis and in sepsis RNA escaping from | |||
damaged tissues/cells may serve as an endogenous ligand for TLR3 thereby | |||
modulating immune responses. This study addressed the hypothesis that TLR3 might Β | |||
regulate mitochondrial function in cultured human hepatocytes. HepG2 cells were | regulate mitochondrial function in cultured human hepatocytes. HepG2 cells were | ||
exposed to TLR-3 ligand (dsRNA--polyinosine-polycytidylic acid; Poly I:C) and | exposed to TLR-3 ligand (dsRNA--polyinosine-polycytidylic acid; Poly I:C) and | ||
| Line 20: | Line 17: | ||
activation and by no major alterations in cellular or mitochondrial | activation and by no major alterations in cellular or mitochondrial | ||
ultrastructure. | ultrastructure. | ||
|keywords=Toll-like receptor; Cyclosporine A; Mitochondrial permeability transition; Mitochondrial respiration; Caspase | |keywords=Toll-like receptor; Cyclosporine A; Mitochondrial permeability transition; Mitochondrial respiration; Caspase; HepG2 | ||
|mipnetlab=CH Bern Djafarzadeh S | |mipnetlab=CH Bern Djafarzadeh S | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration | |||
|organism=Human | |organism=Human | ||
|tissues= | |tissues=Liver | ||
|preparations=Permeabilized | |preparations=Permeabilized cells | ||
|enzymes=Complex I, Complex II; | |enzymes=Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase | ||
|couplingstates=LEAK, OXPHOS | |||
|pathways=N, S, CIV, ROX | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional=Virus, CH, | |||
}} | }} | ||
Latest revision as of 04:26, 29 February 2020
| Djafarzadeh S, Vuda M, Takala J, Ochs M, Jakob SM (2011) Toll-like receptor-3-induced mitochondrial dysfunction in cultured human hepatocytes. Mitochondrion 11:83-8. |
Djafarzadeh S, Vuda M, Takala J, Ochs M, Jakob SM (2011) Mitochondrion
Abstract: Several studies have shown the presence of liver mitochondrial dysfunction during sepsis. TLR3 recognizes viral double-stranded RNA and host endogenous cellular mRNA released from damaged cells. TLR3 ligand amplifies the systemic hyperinflammatory response observed during sepsis and in sepsis RNA escaping from damaged tissues/cells may serve as an endogenous ligand for TLR3 thereby modulating immune responses. This study addressed the hypothesis that TLR3 might regulate mitochondrial function in cultured human hepatocytes. HepG2 cells were exposed to TLR-3 ligand (dsRNA--polyinosine-polycytidylic acid; Poly I:C) and mitochondrial respiration was measured. Poly I:C induced a reduction in maximal mitochondrial respiration of human hepatocytes which was prevented partially by preincubation with cyclosporine A (a mitochondrial permeability transition pore-opening inhibitor). Poly-I:C induced activation of NF-ΞΊB, and the mitochondrial dysfunction was accompanied by caspase-8 but not caspase-3 activation and by no major alterations in cellular or mitochondrial ultrastructure. β’ Keywords: Toll-like receptor; Cyclosporine A; Mitochondrial permeability transition; Mitochondrial respiration; Caspase; HepG2
β’ O2k-Network Lab: CH Bern Djafarzadeh S
Labels: MiParea: Respiration
Organism: Human
Tissue;cell: Liver
Preparation: Permeabilized cells
Enzyme: Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase
Coupling state: LEAK, OXPHOS Pathway: N, S, CIV, ROX HRR: Oxygraph-2k
Virus, CH
