Thyroid hormone-induced oxidative stress triggers nuclear factor-κB activation and cytokine gene expression in rat liver

Tapia, Gladys; Fernández, Virgínia; Varela, Patricia; Cornejo, Pamela; Guerrero, Julia; Videla, Luis A.

doi:10.1016/s0891-5849(03)00209-0

Cited by 61 publications

(61 citation statements)

References 44 publications

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“…However, in other pathophysiological conditions, it has been found that oxidative stress is associated with increased mRNA levels of TNF-α, IL-10, MMP-2 and MMP-9 (Rajagopalan et al 1996;Tapia et al 2003). The differences between the findings obtained here and those present in the literature may be due to the fact that development of oxidative stress might induce different cellular responses, depending on the level of free oxygen radicals achieved and the time of exposure (Droge 2002;Fernandez et al 2006).…”

Section: Resultscontrasting

confidence: 63%

Copper decreases gene expression of TNF-α, IL-10, and of matrix metalloproteinases MMP-2 and MMP-9 in isolated perfused rat livers

et al. 2007

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Abstract:Copper is known to induce oxidative stress in a number of models. It was shown that many pathophysiological events were associated with oxidative stress. Further, oxidative stress can increase gene expression of cytokines and of metalloproteinases. We previously found that copper toxic effects in isolated perfused rat livers were associated with significant oxidative stress (as assessed by lipid peroxidation, protein oxidation and oxidative DNA damage, particularly at concentration of 0.03 mM of Cu 2+ in the perfusate). Here we investigated gene expression of tumor necrosis factor-alpha (TNF-α), interleukin-10 (IL-10), matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) in frozen liver tissue samples by the real-time PCR assay. Compared to controls, copper at concentration of 0.01 mM did not affect gene expression of TNF-α, IL-10, MMP-2 and MMP-9, whereas copper at concentration of 0.03 mM significantly decreased gene expression of all the four TNF-α, IL-10, MMP-2 and MMP-9 by 69%, 81%, 43%, and 62%, respectively. These results suggest that copper-induced oxidative stress in the isolated rat liver can lead to the suppression of gene expression. Because TNF-α and metalloproteinases are involved also in liver regeneration, the suppression of these genes by copper may be one of the mechanisms by which acute intoxication of animals and humans with copper may impair regenerative capability of the liver.

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Section: Resultscontrasting

confidence: 63%

Copper decreases gene expression of TNF-α, IL-10, and of matrix metalloproteinases MMP-2 and MMP-9 in isolated perfused rat livers

et al. 2007

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“…These pretreatments also markedly reduced liver glutathione (GSH) depletion and the enhancement in biliary glutathione disulfide efflux by T 3 , supporting the involvement of oxidative stress in the effects elicited by TH (Fernández et al, 2002). T 3 -induced TNF-α response is paralleled by activation of hepatic nuclear factor-κB (NF-κB), as assessed by electrophoretic mobility shift assay, which is suppressed by α-tocopherol, N-acetylcysteine, and GdCl 3 (Tapia et al, 2003). In agreement with the crucial role of NF-κB in controlling the transcriptional activation of cytokine-encoding genes (Tsukamoto, 2002;Dröge 2002), livers from hyperthyroid animals with enhanced NF-κB DNA binding show induced mRNA expression of TNF-α and interleukin (IL)-10, which correlates with increases in the serum levels of the cytokines (Tapia et al, 2003).…”

Section: Redox Regulation Of Gene Expression By Thyroid Hormonementioning

confidence: 75%

“…T 3 -induced TNF-α response is paralleled by activation of hepatic nuclear factor-κB (NF-κB), as assessed by electrophoretic mobility shift assay, which is suppressed by α-tocopherol, N-acetylcysteine, and GdCl 3 (Tapia et al, 2003). In agreement with the crucial role of NF-κB in controlling the transcriptional activation of cytokine-encoding genes (Tsukamoto, 2002;Dröge 2002), livers from hyperthyroid animals with enhanced NF-κB DNA binding show induced mRNA expression of TNF-α and interleukin (IL)-10, which correlates with increases in the serum levels of the cytokines (Tapia et al, 2003). Upregulation of the IL-1α gene also occurred after T 3 administration, a response that may be due to TNF-α induction (Tapia et al, 2003).…”

Section: Redox Regulation Of Gene Expression By Thyroid Hormonementioning

confidence: 99%

The role of thyroid hormone calorigenesis in the redox regulation of gene expression

et al. 2006

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Thyroid hormone (TH; 3,3 , ,5-triiodothyronine, T 3 ) is required for the normal function of most tissues, with major effects on O 2 consumption and metabolic rate. These are due to transcriptional activation of respiratory genes through the interaction of T 3 -liganded TH receptors with TH response elements or the activation of intermediate factors, with the consequent higher production of reactive O 2 species (ROS) and antioxidant depletion. T 3 -induced oxidative stress in the liver triggers the redox upregulation of the expression of cytokines (tumor necrosis factor-α [TNF-α], interleukin-10), enzymes (inducible nitric oxide synthase, manganese superoxide dismutase), and anti-apoptotic proteins (Bcl-2), via a cascade initiated by TNF-α produced by Kupffer cells, involving inhibitor of κB phosphorylation and nuclear factor-κB activation. Thus, TH calorigenesis triggers an expression pattern that may represent an adaptive mechanism to re-establish redox homeostasis and promote cell survival under conditions of ROS toxicity secondary to TH-induced oxidative stress. Mechanisms of expression of respiratory and redox-sensitive genes may be functionally integrated, which could be of importance to understand the complexities of TH action and the outcome of thyroid gland dysfunction.

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“…Over the past few years increasing evidence has been raised which suggests several nongenomic effects of thyroid hormone , such as the stimulation of plasma membrane transport (Huang et al 1999, Incerpi et al 1999, the modulation of enzyme activities (adenylate cyclase, Ca 2+ -ATPase; Davis et al 1989, Sakaguchi et al 1996, the regulation of mitochondrial processes (Goglia et al 1999), acute changes in the electrical properties of the cell membrane (Ribeiro et al 1998, Sundquist et al 1992, the activation of signal transduction pathways (Lanni et al 1994, Szabo et al 1996, Lin et al 1999a) and the activation of nuclear factor-B by the induction of oxidative stress (Tapia et al 2003).…”

Section: Introductionmentioning

confidence: 99%

Nongenomic effect of thyroid hormone on free-radical production in human polymorphonuclear leukocytes

Mezősi¹,

Szabó²,

Nagy³

et al. 2005

Journal of Endocrinology

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Over the past few years increasing evidence has suggested the nongenomic effects of thyroid hormone, such as the activation of the signal transduction pathways and the activation of nuclear factor-B by the induction of oxidative stress. The present study was undertaken to investigate the effect of thyroid hormone on human polymorphonuclear leukocytes (PMNLs) which are known as important sources of reactive oxygen species in the circulation. The production of superoxide anion (O 2 ) and the activity of myeloperoxidase were determined in the presence and absence of several inhibitors of the signalling pathway. -Thyroxine (T 4 ), L-3,5,3 -tri-iodothyronine (T 3 ) and L-3,5-di-iodothyronine (T 2 ) stimulated O 2 production in PMNLs in a dose-dependent manner within a few minutes of addition to cells. Thyroid hormone-stimulated O 2 production was partially inhibited by pertussis toxin, an inhibitor of GTP-binding G protein, and was completely abolished by the protein kinase C inhibitors calphostin C and Ro-32-0432, and by a calcium chelator (BAPTA; bis-(o-aminophenoxy)ethane-N,N,N ,N -tetraacetic acid). Thyroid hormone stimulated myeloperoxidase activity and induced 125 I incorporation into PMNLs. Furthermore, thyroid hormone pre-incubation enhanced O 2 production for n-formyl-methionyl-leucylphenylalanine (FMLP) stimulation. In conclusion, novel nongenomic actions of thyroid hormone, the induction of superoxide anion production and the stimulation of myeloperoxidase activity in PMNLs were demonstrated. The induction of O 2 production requires calcium and is mediated by a pertussis toxin-sensitive G protein via stimulation of protein kinase C(s). These results suggest the existence of a membrane-bound binding site for thyroid hormone in PMNLs and a physiological role for thyroid hormone in the cellular defence mechanisms by stimulating free-radical production.

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Thyroid hormone-induced oxidative stress triggers nuclear factor-κB activation and cytokine gene expression in rat liver

Cited by 61 publications

References 44 publications

Copper decreases gene expression of TNF-α, IL-10, and of matrix metalloproteinases MMP-2 and MMP-9 in isolated perfused rat livers

Copper decreases gene expression of TNF-α, IL-10, and of matrix metalloproteinases MMP-2 and MMP-9 in isolated perfused rat livers

The role of thyroid hormone calorigenesis in the redox regulation of gene expression

Nongenomic effect of thyroid hormone on free-radical production in human polymorphonuclear leukocytes

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