Difference between revisions of "Regueira 2009 Liver Int"
| Line 1: | Line 1: | ||
{{Publication | {{Publication | ||
|title= | |title=Regueira T, Lepper PM, Brandt S, Ochs M, Vuda M, Takala J, Jakob SM, Djafarzadeh S (2009) Hypoxia inducible factor-1alpha induction by tumour necrosis factor-alpha, but not by toll-like receptor agonists, modulates cellular respiTomas Regueira, Philipp M Lepper, Sebastian Brandt, Matthias Ochs, Madhusudanarao Vuda, Jukka Takala, Stephan M Jakob, Siamak Djafarzadehration in cultured human hepatocytes. Liver Int.10:1582-1592. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/19744167Β 19744167] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/19744167Β 19744167] | ||
|authors=Regueira T, Lepper PM, Brandt S, Ochs M, Vuda M, Takala J, Jakob SM, Djafarzadeh S | |authors=Regueira T, Lepper PM, Brandt S, Ochs M, Vuda M, Takala J, Jakob SM, Djafarzadeh S | ||
Revision as of 17:33, 5 August 2011
| Regueira T, Lepper PM, Brandt S, Ochs M, Vuda M, Takala J, Jakob SM, Djafarzadeh S (2009) Hypoxia inducible factor-1alpha induction by tumour necrosis factor-alpha, but not by toll-like receptor agonists, modulates cellular respiTomas Regueira, Philipp M Lepper, Sebastian Brandt, Matthias Ochs, Madhusudanarao Vuda, Jukka Takala, Stephan M Jakob, Siamak Djafarzadehration in cultured human hepatocytes. Liver Int.10:1582-1592. |
Β» 19744167
Regueira T, Lepper PM, Brandt S, Ochs M, Vuda M, Takala J, Jakob SM, Djafarzadeh S (2009) Liver Int.
Abstract: BACKGROUND/AIMS: Genes encoding for some of the mitochondrial proteins are under the control of the transcriptional factor hypoxia inducible factor-1 alpha (HIF-1 alpha), which can accumulate under normoxic conditions in inflammatory states. The aim of this study was to evaluate the effects of cobalt chloride (CoCl(2), a hypoxia mimicking agent), tumour necrosis factor-alpha (TNF-alpha) and toll-like receptor (TLR) -2, -3 and -4 agonists on HIF-1 alpha accumulation, and further on HIF-1 alpha-mediated modulation of mitochondrial respiration in cultured human hepatocytes.
METHODS: The human hepatoma cell line HepG2 was used in this study. Cells were treated with CoCl(2), TNF-alpha and TLR-2, -3 and -4 agonists. HIF-1 alpha was determined by Western blotting and mitochondrial respiration in stimulated cells by high-resolution respirometry.
RESULTS: CoCl(2), TNF-alpha and TLR agonists induced the expression of HIF-1 alpha in a time-dependent fashion. TNF-alpha and CoCl(2), but not TLR agonists, induced a reduction in complex I-, II- and IV-dependent mitochondrial oxygen consumption. TNF-alpha-associated reduction of cellular oxygen consumption was abolished through inhibition of HIF-1 alpha activity by chetomin (CTM). Pretreatment with cyclosporine A prevented CoCl(2)-induced reduction of complex I- and II-dependent mitochondrial oxygen consumption and TNF-alpha-induced reduction of complex-I-dependent respiration, implicating the involvement of the mitochondrial permeability transition pore openings. TNF-alpha and TLR-2, -3 and -4 agonists induced the expression of vascular endothelial growth factor, which was partially abolished by the blockage of HIF-1 alpha with CTM.
CONCLUSIONS: The data suggest that HIF-1 alpha modulates mitochondrial respiration during CoCl(2) and TNF-alpha stimulation, whereas it has no effect when induced with TLR-2, -3 and -4 agonists.
β’ O2k-Network Lab: CH Bern Djafarzadeh S
Labels:
Stress:Hypoxia Organism: Human Tissue;cell: Hepatocyte; Liver"Hepatocyte; Liver" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property.
HRR: Oxygraph-2k
CTM; HIF-1Ξ±; high-resolution respirometry; mitochondria; MyD88; TLRs; TNF-Ξ±; VEGF
