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      Thyroid Hormone and Tissue Repair: New Tricks for an Old Hormone?

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          Abstract

          Although the role of thyroid hormone during embryonic development has long been recognized, its role later in adult life remains largely unknown. However, several lines of evidence show that thyroid hormone is crucial to the response to stress and to poststress recovery and repair. Along this line, TH administration in almost every tissue resulted in tissue repair after various injuries including ischemia, chemical insults, induction of inflammation, or exposure to radiation. This novel action may be of therapeutic relevance, and thyroid hormone may constitute a paradigm for pharmacologic-induced tissue repair/regeneration.

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          Rapid nongenomic actions of thyroid hormone.

          K K Liao, Tae-Hwan Kim, Aaron T. Scanlan … (2006)
          The binding of thyroid hormone to the thyroid hormone receptor (TR) mediates important physiological effects. However, the transcriptional effects of TR mediated by the thyroid response element (TRE) cannot explain many actions of thyroid hormone. We postulate that TR can initiate rapid, non-TRE-mediated effects in the cardiovascular system through cross-coupling to the phosphatidylinositol 3-kinase (PI3-kinase)/protein kinase Akt pathway. In vascular endothelial cells, the predominant TR isoform is TRalpha1. Treatment of endothelial cells with L-3,5,3'-triiodothyronine (T3) increased the association of TRalpha1 with the p85alpha subunit of PI3-kinase, leading to the phosphorylation and activation of Akt and endothelial nitric oxide synthase (eNOS). The activation of Akt and eNOS by T3 was abolished by the PI3-kinase inhibitors, LY294002 and wortmannin, but not by the transcriptional inhibitor, actinomycin D. To determine the physiological relevance of this PI3-kinase/Akt pathway, we administered T3 to mice undergoing transient focal cerebral ischemia. Compared with vehicle, a single bolus infusion of T3 rapidly increased Akt activity in the brain, decreased mean blood pressure, reduced cerebral infarct volume, and improved neurological deficit score. These neuroprotective effects of T3 were greatly attenuated or absent in eNOS-/- and TRalpha1-/-beta-/- mice and were completely abolished in WT mice pretreated with LY294002 or a T3 antagonist, NH-3. These findings indicate that the activation of PI3-kinase/Akt pathways can mediate some of the rapid, non-TRE effects of TR and suggest that the activation of Akt and eNOS contributes to some of the acute vasodilatory and neuroprotective effects of thyroid hormone.
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            The FoxO3/type 2 deiodinase pathway is required for normal mouse myogenesis and muscle regeneration.

            Monica Dentice, Alessandro Marsili, Raffaele Ambrosio … (2010)
            The active thyroid hormone 3,5,3' triiodothyronine (T3) is a major regulator of skeletal muscle function. The deiodinase family of enzymes controls the tissue-specific activation and inactivation of the prohormone thyroxine (T4). Here we show that type 2 deiodinase (D2) is essential for normal mouse myogenesis and muscle regeneration. Indeed, D2-mediated increases in T3 were essential for the enhanced transcription of myogenic differentiation 1 (MyoD) and for execution of the myogenic program. Conversely, the expression of T3-dependent genes was reduced and after injury regeneration markedly delayed in muscles of mice null for the gene encoding D2 (Dio2), despite normal circulating T3 concentrations. Forkhead box O3 (FoxO3) was identified as a key molecule inducing D2 expression and thereby increasing intracellular T3 production. Accordingly, FoxO3-depleted primary myoblasts also had a differentiation deficit that could be rescued by high levels of T3. In conclusion, the FoxO3/D2 pathway selectively enhances intracellular active thyroid hormone concentrations in muscle, providing a striking example of how a circulating hormone can be tissue-specifically activated to influence development locally.
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              Feeding Experiments on tadpoles

              J. F. Gudernatsch (1912)
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Thyroid Res
                Journal ID (iso-abbrev): J Thyroid Res
                Journal ID (publisher-id): JTR
                Title: Journal of Thyroid Research
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2090-8067
                ISSN (Electronic): 2042-0072
                Publication date (Print): 2013
                Publication date (Electronic): 25 February 2013
                Volume: 2013
                Electronic Location Identifier: 312104
                Affiliations
                Department of Pharmacology, University of Athens, 75 Mikras Asias Avenue, Goudi, 11527 Athens, Greece
                Author notes
                *Constantinos Pantos: cpantos@ 123456med.uoa.gr

                Academic Editor: Giorgio Iervasi

                Article
                DOI: 10.1155/2013/312104
                PMC ID: 3596953
                PubMed ID: 23533950
                SO-VID: eee6b156-4466-4a54-9f01-526c733e5b55
                Copyright © Copyright © 2013 Iordanis Mourouzis et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 1 November 2012
                Date accepted : 26 January 2013
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Endocrinology & Diabetes
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes

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