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S Palmero, P De Marco and E Fugassa

ABSTRACT

A polymerase chain reaction (PCR)-based assay was used to evaluate the expression of thyroid hormone receptor β mRNA in Sertoli cells isolated from both prepubertal rat and piglet testes. The expression of an mRNA coding for the functional thyroid hormone receptor β isoform, as established by the PCR assay, agrees with the presence of specific tri-iodothyronine (T3)-binding sites in the Sertoli cell nuclei of both species, as previously evaluated by displacement analysis. The results ratify the existence of a functional T3 receptor in the prepubertal testis and confirm the Sertoli cell as a specific target for thyroid hormone action on the developing testis. On the other hand, in both peripubertal rat (Palmero et al. 1988; Jannini et al. 1990) and piglet (Palmero et al. 1992) testes, high-affinity, low-capacity T3 binding sites have been specifically localised at the Sertoli cell level and TRal mRNA expression has been detected very recently in immature Sertoli cells (Jannini et al. 1994).

The aim of the present work was to test if, in prepubertal Sertoli cells isolated from both immature rat and piglet testes, the expression of an erbAβ mRNA specifically coding for the TR protein could be detected employing an highly sensitive polymerase chain reaction (PCR)-based assay.

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Changhua Shi, Qing Meng and David W Wood

in multiple species . Environmental Toxicology 28 179 – 189 . ( doi:10.1002/tox.20708 ). Grijota-Martínez C Samarut E Scanlan TS Morte B Bernal J 2011 In vivo activity of the thyroid hormone receptor β- and α-selective agonists GC-24 and CO23 on rat

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Pamela Navarrete-Ramírez, Maricela Luna, Carlos Valverde-R and Aurea Orozco

Comparative Endocrinology 135 345 – 357 . ( doi:10.1016/j.ygcen.2003.10.012 ). Mendoza CA Navarrete-Ramírez P Hernández-Puga G Villalobos P Holzer G Laudet V Renaud JP Orozco A 2013 3,5-T 2 is an alternative ligand for the thyroid hormone receptor β1

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V Tassi, L Scarnecchia, A Di Cerbo, M T Pirro, R Di Paola, A Liuzzi, M Torlontano, M Zingrillo, L D’Aloiso and V De Filippis

ABSTRACT

Autoimmune thyroid diseases (AITDs) are clustered in families, but the nature of this clustering is still poorly understood. One possible approach to the identification of genetic factors interacting with the AITDs is the study of the association between polymorphic markers and AITDs themselves. In the present study we have shown an association between an allele of a HindIII restriction fragment length polymorphism (EAβH) intragenic to c-erbAβ, which codes for the thyroid hormone β receptor, and Graves’ disease. This polymorphism can be detected by PCR followed by digestion with the restriction enzyme HindIII. The allelic frequencies were analysed in a panel of DNAs extracted from a population of individuals affected by thyroid disease and originating from southern Italy. A control group (n=120) from the same area was also analysed. The distribution of EAβH alleles was significantly different (P<0·001) in Graves’ disease (n=94) but not in autoimmune thyroiditis (n=60), as compared with controls. Also the distribution of the EAβH genotypes was significantly different in Graves’ patients (P=0·003), as compared with controls, the homozygous state EAβH+/EAβH+ being more frequent in Graves’ patients than in all the other groups. We did not find any association between EAβH genotypes and clinical parameters in Graves’ patients, including eye signs, thyroid volume and level of TSH-binding inhibiting immunoglobulins. Our data support the idea that Graves’ disease is a genetically distinct group within the AITDs.

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Sogol Gachkar, Sebastian Nock, Cathleen Geissler, Rebecca Oelkrug, Kornelia Johann, Julia Resch, Awahan Rahman, Anders Arner, Henriette Kirchner and Jens Mittag

It is well established that thyroid hormones are required for cardiovascular functions; however, the molecular mechanisms remain incompletely understood, especially the individual contributions of genomic and non-genomic signalling pathways. In this study, we dissected how thyroid hormones modulate aortic contractility. To test the immediate effects of thyroid hormones on vasocontractility, we used a wire myograph to record the contractile response of dissected mouse aortas to the adrenergic agonist phenylephrine in the presence of different doses of T3 (3,3′,5-triiodothyronine). Interestingly, we observed reduced vasoconstriction under low and high T3 concentrations, indicating an inversed U-shaped curve with maximal constrictive capacity at euthyroid conditions. We then tested for possible genomic actions of thyroid hormones on vasocontractility by treating mice for 4 days with 1 mg/L thyroxine in drinking water. The study revealed that in contrast to the non-genomic actions the aortas of these animals were hyperresponsive to the contractile stimulus, an effect not observed in endogenously hyperthyroid TRβ knockout mice. To identify targets of genomic thyroid hormone action, we analysed aortic gene expression by microarray, revealing several altered genes including the well-known thyroid hormone target gene hairless. Taken together, the findings demonstrate that thyroid hormones regulate aortic tone through genomic and non-genomic actions, although genomic actions seem to prevail in vivo. Moreover, we identified several novel thyroid hormone target genes that could provide a better understanding of the molecular changes occurring in the hyperthyroid aorta.

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Maciej Pietrzak and Monika Puzianowska-Kuznicka

conditions the MCL-1 promoter was activated twofold. This indicates that TRβ1, but not TRα1, is crucial for MCL-1 activation by T 3 . Figure 2 Triiodothyronine activates the MCL-1 promoter in the presence of thyroid hormone receptor β1, but not of its α

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Sadako Suzuki, Shigekazu Sasaki, Hiroshi Morita, Yutaka Oki, Daisuke Turiya, Takeshi Ito, Hiroko Misawa, Keiko Ishizuka and Hirotoshi Nakamura

Peroxisome proliferator-activated receptor γ-2 (PPARG2) is a ligand-dependent transcriptional factor involved in the pathogenesis of insulin resistance. In the presence of a ligand, PPARG2 associates with co-activators, while it recruits co-repressors (CoRs) in the absence of a ligand. It has been reported that the interaction of liganded PPARG2 with co-activators is regulated by the amino-terminal A/B domain (NTD) via inter-domain communication. However, the role of the NTD is unknown in the case of the interaction between unliganded PPARG2 and CoRs. To elucidate this, total elimination of the influence of ligands is required, but the endogenous ligands of PPARG2 have not been fully defined. PPARG1-P467L, a naturally occurring mutant of PPARG1, was identified in a patient with severe insulin resistance. Reflecting its very low affinity for various ligands, this mutant does not have transcriptional activity in the PPAR response element, but exhibits dominant negative effects (DNEs) on liganded wild-type PPARG2-mediated transactivation. Using the corresponding PPARG2 mutant, PPARG2-P495L, we evaluated the role of the NTD in the interaction between unliganded PPARG2 and CoRs. Interestingly, the DNE of PPARG2-P495L was increased by the truncation of its NTD. NTD deletion also enhanced the DNE of a chimeric receptor, PT, in which the ligand-binding domain of PPARG2 was replaced with that of thyroid hormone receptor β-1. Moreover, NTD deletion facilitated the in vitro binding of nuclear receptor CoR with wild-type PPARG2, mutant P495L, and the PT chimera (PPARG2-THRB). Inter-domain communication in PPARG2 regulates not only ligand-dependent transactivation but also ligand-independent silencing.

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Richard Keijzer, Piet-Jan E Blommaart, Wil T Labruyère, Jacqueline L M Vermeulen, Behrouz Zandieh Doulabi, Onno Bakker, Dick Tibboel and Wouter H Lamers

-Moura C, Moura E, Kaulbach H, Zakaria M, Lowell B, Radovick S, Liberman MC & Wondisford F 1999 Divergent roles for thyroid hormone receptor β isoforms in the endocrine axis and auditory system. Journal of Clinical Investigation 104 291 –300

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Isabel Castro, Leah Quisenberry, Rosa-Maria Calvo, Maria-Jesus Obregon and Joaquin Lado-Abeal

Monocarboxylate transporter 8 ( MCT8 ); thyroid hormone receptors β ( THRB ), α1 ( THRA1 ), and α2 ( THRA2 ); and retinoid X receptors α ( RXRA ) and β ( RXRB ) gene expression changes between control (n:8) and LPS-treated (n:9) pigs. Relative gene expression is

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Laura Calzà, Mercedes Fernandez and Luciana Giardino

interleukin-1β-mediated decrease of deiodinase type 1 and thyroid hormone receptor β1 mRNA . Journal of Endocrinology 189 37 – 44 . Kwakkel J Wiersinga WM Boelen A 2007 Interleukin-1 beta modulates endogenous thyroid hormone alpha gene