Kupffer-cell activity is essential for thyroid hormone rat liver preconditioning

Tapia, Gladys; Santibáñez, C.; Farias, José Wilson Mourão de; Fuenzalida, Gabriel; Varela, Patricia; Videla, Luis A.; Fernández, Virgínia

doi:10.1016/j.mce.2010.03.014

Cited by 18 publications

(17 citation statements)

References 35 publications

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“…In addition to enzyme inactivation, thyrotoxicosis in mammals results in the stimulation of both synthesis and degradation of protein, with a predominance of degradation, as shown by the increase in protein catabolism, negative nitrogen balance, and the loss of protein from muscle and other body stores (Loeb, 1996). These findings are in accordance with those of Tapia et al who found a higher oxidation of the liver protein and an increase in lipid peroxidation levels in hyperthyroid rats (Tapia et al, 2010).…”

Section: Hyperthyroidism and The Ros-steady Statesupporting

confidence: 93%

The Relationship Between Thyroid States, Oxidative Stress and Cellular Damage

Cano-Europa¹,

Blas-Valdivia²,

Franco-Colín³

et al. 2012

Oxidative Stress and Diseases

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Section: Hyperthyroidism and The Ros-steady Statesupporting

confidence: 93%

The Relationship Between Thyroid States, Oxidative Stress and Cellular Damage

Cano-Europa¹,

Blas-Valdivia²,

Franco-Colín³

et al. 2012

Oxidative Stress and Diseases

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“…Hepatic ischaemic reperfusion injury in rats results in severe liver damage (Fernandez et al 2007a, 2008, Tapia et al 2010. These effects were prevented and even reversed by preconditioning with a single dose of T 3 (Fernandez et al 2007a, 2008, Tapia et al 2010.…”

Section: Thyroid Hormone Metabolism In Tissue-resident Macrophagesmentioning

confidence: 99%

Thyroid hormone metabolism in innate immune cells

Spek

Fliers

Boelen

2017

Journal of Endocrinology

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Thyroid hormone (TH) metabolism and thyroid status have been linked to various aspects of the immune response. There is extensive literature available on the effects of thyroid hormone on innate immune cells. However, only recently have authors begun to study the mechanisms behind these effects and the role of intracellular TH metabolism in innate immune cell function during inflammation. This review provides an overview of the molecular machinery of intracellular TH metabolism present in neutrophils, macrophages and dendritic cells and the role and effects of intracellular TH metabolism in these cells. Circulating TH levels have a profound effect on neutrophil, macrophage and dendritic cell function. In general, increased TH levels result in an amplification of the pro-inflammatory response of these cells. The mechanisms behind these effects include both genomic and non-genomic effects of TH. Besides a pro-inflammatory effect induced by extracellular TH, the cellular response to pro-inflammatory stimuli appears to be dependent on functional intracellular TH metabolism. This is illustrated by the fact that the deiodinase enzymes and in some cell types also thyroid hormone receptors appear to be crucial for adequate innate immune cell function. This overview of the literature suggests that TH metabolism plays an important role in the host defence against infection through the modulation of innate immune cell function.

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“…T 3 preconditioning (0.1 mg/kg) occurs 48 h prior to IR (1 h of partial ischemia followed by 20 h of reperfusion) and is triggered by Kupffer cell activation and induction of transient and moderate liver oxidative stress [12,13,16]. n-3 PUFA supplementation, using a protocol of daily doses of 300 mg/kg during 7 days, also affords significant protection against liver IR injury [14].…”

Section: Introductionmentioning

confidence: 99%