Mechanisms of nongenomic actions of thyroid hormone

Davis, Paul J.; Leonard, Jack L.; Davis, Faith B.

doi:10.1016/j.yfrne.2007.09.003

Cited by 316 publications

(250 citation statements)

References 53 publications

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“…Data discussed in this article indicate that redox regulation of gene transcription by T 3 (i) represents an additional nongenomic mechanism to those reported for different cellular processes, such as stimulation of plasma membrane transport, modulation of enzyme activity and mitochondrial processes, or signal transduction pathways underlying cell surface G protein-coupled T 3 /T 4 membrane-binding site mitogen-activated protein kinases (16,19,21,(85)(86)(87) and (ii) is dependent upon the genomic pathway triggering energy metabolism with ROS production ( Fig. 1; 12).…”

Section: Discussionmentioning

confidence: 79%

“…1; 12). The nongenomic actions of thyroid hormones may in turn influence gene transcription by different pathways involving either antioxidant-sensitive NF-jB, AP-1, and STAT3 activation (67,80) or TR and STAT phosphorylation (19,85). Furthermore, CREB-binding protein and the related protein p300 activating liganded TRs in the classical genomic pathway of T 3 action (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, several thyroid hormone effects that are independent of intranuclear ligand binding by TR are called nongenomic and require either a plasma membrane receptor (integrin aVb3 receptor; Fig. 1) or nuclear receptors located in cytoplasm (TRb1, TRDa1) for signaling (19). T 3 calorigenesis is primarily due to the induction of enzymes related to mitochondrial electron transport and ATP synthesis, catabolism, and some anabolic processes through upregulation of genomic mechanisms (Fig.…”

Section: T 3 -Induced Enhancement Of Liver O 2 Consumption and Oxidatmentioning

confidence: 99%

“…Nongenomic signaling occurring via 3,5-diiodothyronine (3,5-T 2 ) and T 3 may also be operative, leading to allosteric activation of cytochrome c oxidase (21). The net result of the activation of both signaling pathways is the enhancement in the rate of O 2 consumption of target tissues such as liver (22), which may be contributed by secondary processes induced by T 3 such as (i) induction of uncoupling proteins (23); (ii) energy expenditure due to futile cycles coupled to increase in catabolic and anabolic pathways (24); (iii) loss of energy due to higher active cation transport (16,19); and (iv) O 2 equivalents used in the generation of mitochondrial ROS ( Fig. 1; 25, 26).…”

Section: T 3 -Induced Enhancement Of Liver O 2 Consumption and Oxidatmentioning

confidence: 99%

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Hormetic responses of thyroid hormone calorigenesis in the liver: Association with oxidative stress

Videla

2010

IUBMB Life

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SummaryThyroid hormone (L-3,3 0 ,5-triiodothyronine, T 3 ) exerts calorigenic effects by accelerating mitochondrial O 2 consumption through transcriptional activation of respiratory genes, with consequent increased reactive oxygen species (ROS) production. In the liver, ROS generation occurs at different sites of hepatocytes and in the respiratory burst of Kupffer cells, triggering the activation of the transcription factors nuclear factor-jB, signal transducer and activator of transcription 3, and activating protein 1. Under these conditions, the redox upregulation of Kupffer cell-dependent expression of cytokines [tumor necrosis factor-a, interleukin (IL)-1, and IL-6] is achieved, which upon interaction with specific receptors in hepatocytes trigger the expression of antioxidant enzymes (manganese superoxide dismutase, inducible nitric oxide synthase), antiapoptotic proteins (Bcl-2), and acute-phase proteins (haptoglobin, b-fibrinogen). These responses and the promotion of hepatocyte and Kupffer cell proliferation observed represent hormetic effects re-establishing redox homeostasis, promoting cell survival, and protecting the liver against ischemia-reperfusion (IR) injury. It is proposed that hormesis underlying T 3 action may constitute a novel preconditioning strategy for IR injury during liver surgery in man or in liver transplantation using reduced-size grafts from living donors, considering that (i) with the exception of the controversial ischemic preconditioning, all other studied strategies have failed to reach the clinical setting and (ii) T 3 is a well-tolerated therapeutic agent that either lacks major adverse effects or has minimal and controlled side effects. IUBMBIUBMB Life, 62(6): [460][461][462][463][464][465][466] 2010

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Section: Discussionmentioning

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Section: T 3 -Induced Enhancement Of Liver O 2 Consumption and Oxidatmentioning

confidence: 99%

Section: T 3 -Induced Enhancement Of Liver O 2 Consumption and Oxidatmentioning

confidence: 99%

See 2 more Smart Citations

Hormetic responses of thyroid hormone calorigenesis in the liver: Association with oxidative stress

Videla

2010

IUBMB Life

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“…Particularly, nongenomic TH effects were reported in mammals, involving TH receptors other than TR (Davis et al, 2007;Scanlan et al, 2004). However, the mode of action of those receptors is not well understood yet Scanlan et al, 2004).…”

Section: Tr Is the Th Receptor In Chordatesmentioning

confidence: 99%

The history of a developmental stage: Metamorphosis in chordates

Paris

Laudet

2008

Genesis

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Summary: Metamorphosis displays a striking diversity in chordates, a deuterostome phylum that comprises vertebrates, urochordates (tunicates), and cephalochordates (amphioxus). In anuran amphibians, the tadpole loses its tail, develops limbs, and undergoes profound changes at the behavioral, physiological, biochemical, and ecological levels. In ascidian tunicates, the tail is lost and the head tissues are drastically remodeled into the adult animal, whereas in amphioxus, the highly asymmetric larva transforms into a relatively symmetric adult. This wide diversity has led to the proposal that metamorphosis evolved several times independently in the different chordate lineages during evolution. However, the molecular mechanisms involved in metamorphosis are largely unknown outside amphibians and teleost fishes, in which metamorphosis is regulated by the thyroid hormones (TH) T 3 and T 4 binding to their receptors (thyroid hormone receptors). In this review, we compare metamorphosis in chordates and then propose a unifying definition of the larva-to-adult transition, based on the conservation of the role of THs and some of their derivatives as the main regulators of metamorphosis. According to this definition, all chordates (if not, all deuterostomes) have a homologous metamorphosis stage during their postembryonic development. The intensity and the nature of the morphological remodeling varies extensively among taxa, from drastic remodeling like in some ascidians or amphibians to more subtle events, as in mammals. genesis 46:657-672,

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Mechanisms of Endocrine System Function

Khetan¹

2014

Endocrine Disruptors in the Environment

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HORMONAL AXES 31disruptors are able to disturb hormonal homeostasis of organisms by mimicking the hormonal activity of the natural hormones.The lipophilic steroid and thyroid hormones (THs) simply diffuse across the plasma membrane and out of the cell down a concentration gradient to readily enter cells to interact with cytoplasmic or nuclear receptors. Hypothalamus-Pituitary-Gonad (HPG) AxisThe primary function of the HPG axis in vertebrates is to facilitate the production of germ cells in males and to coordinate reproductive events such as ovulation, pregnancy, and lactation in females. In addition to its function in adult animals, the HPG axis regulates the differentiation of the sex-specific phenotype during early development, where sex steroids play a pivotal role.The hypothalamus, located at the base of the brain, acts as a central processor for regulating the endocrine system by maintaining homeostasis of a variety of physiologic functions. It initiates the secretion of gonadotropin-releasing hormone (GnRH) in a pulsatile manner into the blood. At the anterior pituitary, the GnRH diffuses to its target cells, called gonadotropes. The gonadotrope cells synthesize/secrete the gonadotropins, LH, and FSH. In response to GnRH stimulation, the gonadotropes quickly release the gonadotropins from the pituitary gland into the general circulating system, and target the gonads (ovary or testis). At the gonad, gonadotropins drive the synthesis of steroid hormones via steroidogenesis and production of sperm and ova via gametogenesis. Sertoli and Leydig (testis) cells and theca and granulosa (ovary) cells have receptors for LH and FSH, and produce steroid hormones including estrogen and testosterone, as well as other factors (such as inhibin B), which induce a direct effect on hormone-responsive tissues. The steroid hormones, in turn, regulate GnRH production in the hypothalamus (and, therefore, secretion of pituitary gonadotropins). The hypothalamus and pituitary operate under negative feedback control regulated by levels of gonadotropins and steroids. This control route, hypothalamus → pituitary → gonad, is called the HPG axis ( Fig. 2.2), and is one of several highly conserved hypothalamic-pituitary-hormonal axes in the vertebrates.During puberty, the HPG axis is activated, leading to increases in LH, FSH, and sex steroids (testosterone and estradiol) levels (Grumbach and Styne, 2003). LH and FSH play important roles in the menstrual cycle. LH stimulates production of testosterone from Leydig cells and secretion by the follicle. FSH stimulates the Sertoli cells, causing the testes to produce a hormone that regulates sperm production. Sex steroids then act upon steroid hormone receptors, primarily estrogen receptors (ERs), androgen receptors (ARs), and progesterone receptors (PRs), that are widely expressed in target tissues, including the reproductive tract and genitalia, breast, and other organ systems.Under the control of FSH, androgen is converted to estrogen by aromatizing the A ring of the steroid molecule throu...

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Mechanisms of nongenomic actions of thyroid hormone

Cited by 316 publications

References 53 publications

Hormetic responses of thyroid hormone calorigenesis in the liver: Association with oxidative stress

Hormetic responses of thyroid hormone calorigenesis in the liver: Association with oxidative stress

The history of a developmental stage: Metamorphosis in chordates

Mechanisms of Endocrine System Function

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