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Editorial. Nongenomic effects of thyroid hormones in central nervous system and skeletal muscle: from zebrafish to man
No full textThyroid Hormones. From Molecular Signaling to Human Disease: An Update
No full textThis Thematic Issue presents reviews of recent studies on effects of thyroid hormones and certain metabolites that are linked to human diseases, providing a general update of the topic. I have been the guest editor for thematic issues of IEMAMC for three times, in 2006, 2011 and 2015, and over these 10 years my knowledge of the nongenomic effects of thyroid hormone has improved considerably. First issue was dedicated to the nongenomic effects of various hormones endowed with classical nuclear receptors, and included a chronology of the earliest reported nongenomic effects of thyroid hormones. Second issue was centered on thyroid hormone nongenomic mechanisms in skeletal muscle and nerve cells, mainly, but not exclusively, dealing with effects mediated by integrin alphaVbeta3. In the current issue, the coverage of thyroid hormone actions is wider, including also nuclear classical effects, the cognitive processes and effects of some hormone metabolites that are particularly interesting from pharmacological point of view. Why? When a new surprising discovery is published, such as the seminal paper by Bergh et al., in 2005, showing that the integrin alphaVbeta3 was the long-searched plasma membrane receptor for thyroid hormones, it can of course dominate the scenery for years, and other researchers in this field will use this new piece of information in their studies to understand the physio-pathological effects of thyroid hormones. The Bergh et al. paper showed that binding by thyroxine to the integrin alphaVbeta3 gives rise to a downstream signaling that causes MAPK activation and tumor cell proliferation. This has so to say been the ‘Big Bang’ of nongenomic effects of thyroid hormones. After ten years of the integrin story, we can now observe how many things have changed in our knowledge about the role of thyroid hormones in animal physiology. However, actually the integrin story began before alphaVbeta3 was recognized as a plasma membrane thyroid hormone receptor. The group of Davis and Davis showed, in 2004, that various effects of thyroid hormone on the actions of epidermal growth factor and transforming growth factor-alpha were mediated by cAMP-dependent protein kinase II. The crosstalk between thyroid hormones and growth factors reported in that paper would eventually lead to the integrin; alphaVbeta3 was ‘in nuce’ although it was not clear at that time. Now, this interaction of thyroid hormones with growth factors is coming of age and may lead us far, to different and still unknown aspects of physiology and pathology, as it can be observed from some of the contributions in this issue
Editorial. The extranuclear life of the nuclear receptor hormone family: New therapeutic possibilities
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Nongenomic effects of thyroid hormones on ion transport
No full textExtranuclear or nongenomic effects of thyroid hormone are unaffected by the inhibitors of protein synthesis, and their time course cannot be explained by the interaction of the hormone molecule with nuclear receptors. Their site of action has been localized at the plasma membrane, but also at the cytoplasm and organelles such as the mitochondria. In particular thyroid hormone has been reported to activate, by both genomic and non genomic mechanism, the Ca2+-ATPase, an ion pump that removes calcium from the cytosol and stores it in the sarcoplasmic reticulum. The decrease in intracellular Ca2+ generated during the systole leads to cardiac muscle relaxation. Given to all these important effects on the cardiovascular system, T3 can be also envisaged as a potent novel therapeutic agent as a inotropic drug. Thyroid hormone is also a major regulator of the Na/K-ATPase activity in several tissues. L-T3 and its analog 3,5-diiodothyronine give rise to a fast inhibition of the Na+/K+-ATPase activity in chick embryo hepatocytes, whereas L-T4 appears to be ineffective. The Na/H exchanger, activated by the thyroid hormone by both genomic and nongenomic mechanism, is a ubiquitous plasma membrane integral protein exchanging extracellular Na+ with cytoplasmic H+ ions according to the concentration gradient; it does not require energy supply, but depends on the Na+/K+-ATPase. Some of these effects are mediated by PKC and MAPK pathway, likely interfaces between genomic and nongenomic effects of thyroid hormones. The extranuclear effects should be taken into account when considering appropriate therapeutic intervention based on thyroid hormone both for their possible reinforcement of the nuclear effects and for their fast time onset, that might be of clinical relevance particularly for the cardiovascular system
Annual variations in the binding of insulin to hepatic membranes of the frog Rana esculenta
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Effect of atrial natriuretic peptide on reactive oxygen species-induced by hydrogen peroxide in THP-1 monocytes: role in cell growth, migration and cytokine release.
No full text"tAtrial natriuretic peptide (ANP), a cardiovascular hormone, elicits different biological actions in theimmune system. The aim of the present study was to investigate in THP-1 monocytes the ANP effecton hydrogen peroxide (H2O2)-induced Reactive Oxygen Species (ROS), cell proliferation and migration.A significant increase of H2O2-dependent ROS production was induced by physiological concentration ofANP (10−10M). The ANP action was partially affected by cell pretreatment with PD98059, an inhibitor ofmitogen activated-protein kinases (MAPK) as well as by wortmannin, an inhibitor of phosphatidylinositol3-kinase (PI3K) and totally suppressed by diphenylene iodonium (DPI), an inhibitor of the enzyme nico-tinamide adenine dinucleotide phosphate (NADPH) oxidase. The hormone effect was mimicked by cANFand an ANP\/NPR-C signaling pathway was studied using pertussis toxin (PTX). A significant increase ofH2O2-induced cell migration was observed after ANP (10−10M) treatment, conversely a decrease of THP-1proliferation, due to cell death, was found. Both ANP actions were partially prevented by DPI. Moreover,H2O2-induced release of IL-9, TNF-, MIP-1 and MIP-1 was not counteracted by DPI, whereas no effectwas observed in any experimental condition for both IL-6 and IL-1. Our results support the view thatANP can play a key role during the inflammatory process.
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