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      Thyroid Hormones and Growth in Health and Disease

      review-article
      Author(s): 1
      Publication date (Electronic):
      Journal: Journal of Clinical Research in Pediatric Endocrinology
      Publisher: Galenos Publishing
      Keywords: Thyroid, growth, children

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          Abstract

          Thyroid hormones regulate growth by several mechanisms. In addition to their negative feedback effect on the stimulatory hormones thyrotropin-releasing hormone (TRH) and thyrotropin (TSH), thyroid hormones also regulate their receptors in various physiological and pathological conditions. Up-regulation and down-regulation of the thyroid receptors fine-tune the biological effects exerted by the thyroid hormones. Interestingly, the deiodinase enzyme system is another intrinsic regulator of thyroid physiology that adjusts the availability of thyroid hormones to the tissues, which is essential for normal growth and development. Almost all chronic diseases of childhood impair growth and development. Every disease may have a unique mechanism to halt linear growth, but reduced serum concentration or diminished local availability of thyroid hormones seems to be a common pathway. Therefore, the effects of systemic diseases on thyroid physiology must be taken into consideration in the evaluation of growth retardation in affected children.

          Conflict of interest:None declared.

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          Biochemistry, cellular and molecular biology, and physiological roles of the iodothyronine selenodeiodinases.

          Antonio Bianco, Domenico Salvatore, Balázs Gereben … (2002)
          The goal of this review is to place the exciting advances that have occurred in our understanding of the molecular biology of the types 1, 2, and 3 (D1, D2, and D3, respectively) iodothyronine deiodinases into a biochemical and physiological context. We review new data regarding the mechanism of selenoprotein synthesis, the molecular and cellular biological properties of the individual deiodinases, including gene structure, mRNA and protein characteristics, tissue distribution, subcellular localization and topology, enzymatic properties, structure-activity relationships, and regulation of synthesis, inactivation, and degradation. These provide the background for a discussion of their role in thyroid physiology in humans and other vertebrates, including evidence that D2 plays a significant role in human plasma T(3) production. We discuss the pathological role of D3 overexpression causing "consumptive hypothyroidism" as well as our current understanding of the pathophysiology of iodothyronine deiodination during illness and amiodarone therapy. Finally, we review the new insights from analysis of mice with targeted disruption of the Dio2 gene and overexpression of D2 in the myocardium.
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            A transcriptional co-repressor that interacts with nuclear hormone receptors.

            J D Chen, R Evans (1995)
            Transcriptional silencing mediated by nuclear receptors is important in development, differentiation and oncogenesis. The mechanism underlying this effect is unknown but is one key to understanding the molecular basis of hormone action. Here we identify a receptor-interacting factor, SMRT, as a silencing mediator (co-repressor) for retinoid and thyroid-hormone receptors. SMRT is a previously undiscovered protein whose association with receptors both in solution and bound to DNA-response elements is destabilized by ligand. The interaction with mutant receptors correlates with their transcriptional silencing activities. In vivo, SMRT functions as a potent co-repressor, and a GAL4 DNA-binding domain fusion of SMRT behaves as a frank repressor of a GAL4-dependent reporter. Together, our results identify a new class of cofactors which may be important mediators of hormone action.
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              Sequence and characterization of a coactivator for the steroid hormone receptor superfamily.

              S Oñate, S. Tsai, M Tsai … (1995)
              A yeast two-hybrid system was used to identify a protein that interacts with and enhances the human progesterone receptor (hPR) transcriptional activity without altering the basal activity of the promoter. Because the protein stimulated transactivation of all the steroid receptors tested, it has been termed steroid receptor coactivator-1 (SRC-1). Coexpression of SRC-1 reversed the ability of the estrogen receptor to squelch activation by hPR. Also, the amino terminal truncated form of SRC-1 acted as a dominant-negative repressor. Together, these results indicate that SRC-1 encodes a coactivator that is required for full transcriptional activity of the steroid receptor superfamily.
              Article 0 comments Cited 184 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Clin Res Pediatr Endocrinol
                Journal ID (publisher-id): JCRPE
                Title: Journal of Clinical Research in Pediatric Endocrinology
                Publisher: Galenos Publishing
                ISSN (Print): 1308-5727
                ISSN (Electronic): 1308-5735
                Publication date (Print): June 2011
                Publication date (Electronic): 8 June 2011
                Volume: 3
                Issue: 2
                Pages: 51-55
                Affiliations
                [1 ] Uludağ University Faculty of Medicine, Division of Pediatric Endocrinology, Bursa, Turkey
                Article
                Publisher Item ID: 92
                DOI: 10.4274/jcrpe.v3i2.11
                PMC ID: 3119440
                PubMed ID: 21750631
                SO-VID: e451de3c-8b94-42b1-a16d-2197b6a81f28
                Copyright © © Journal of Clinical Research in Pediatric Endocrinology, Published by Galenos Publishing.
                License:

                This is an open-access article distributed under the terms of 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 : 27 January 2011
                Date accepted : 19 February 2011
                Categories
                Subject: Review

                ScienceOpen disciplines: Pediatrics
                Keywords: children,growth,thyroid
                Data availability:
                ScienceOpen disciplines: Pediatrics
                Keywords: children, growth, thyroid

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