Antipeptide polyclonal antibodies specifically recognize each human thyroid hormone receptor isoform.

Falcone, M; Miyamoto, Takahide; Fierro-Renoy, Francisco; Macchia, Enrico; DeGroot, Leslie J.

doi:10.1210/endo.131.5.1425440

Cited by 81 publications

(25 citation statements)

References 29 publications

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“…different from the control stained with normal rabbit serum. We have reported similar data obtained in adult rat heart utilizing the same antibodies for immunohistochemical analysis (26).…”

Section: Resultssupporting

confidence: 72%

“…The characterization of these antipeptide polyclonal antibodies, competition studies (preadsorbing each antibody with the specific peptide or with the whole protein expressed in Escherichia coli) and immunoprecipitation analysis (immunoprecipitation of the protein translated in vitro and of the thyroid hormone receptor expressed in E. coli) were reported previously (26,27). Alpha-2-431 antibody activity could be blocked by an excess amount of immunizing peptide and by TR alpha-2 expressed in B. coli in both ELISA and western blotting analyses, but only a partial competition was obtained in our immuno¬ histochemical studies.…”

Section: Methodsmentioning

confidence: 99%

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Evaluation of the ontogeny of thyroid hormone receptor isotypes in rat brain and liver using an immunohistochemical technique

Falcone

Miyamoto²,

Fierro-Renoy³

et al. 1994

European Journal of Endocrinology

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We performed an immunohistochemical study on rat brain and liver during fetal and neonatal life using rabbit antipeptide polyclonal antibodies able to recognize each thyroid hormone receptor (TR) isoform. The expression of TR alpha-1, alpha-2 and beta-1 proteins from 14 days of gestation to 21 days after birth was evaluated. Frozen tissues from 14 (F14), 17 (F17) and 21 (F21)-day-old fetuses and from 5 (N5), 16 (N16) and 21 (N21)-day old newborn rats were stained with anti-TR antibodies using an avidin-biotin-peroxidase system. The antipeptide antibodies utilized in the present study were characterized previously: alpha-144 antibody recognizes both TR alpha-1 and alpha-2; alpha-2-431 antibody is specific for TR variant alpha-2, and beta-62 antibody specifically reacts with the TR beta-1 isoform. The expression of TR alpha-1 was deduced by comparing the staining obtained with alpha-144 and alpha-2-431 antibodies. We demonstrated that each TR isoform is expressed in rat brain from 14 days of gestation and that the alpha isoform was predominant in the early stage. The three TR isoforms were expressed in both neural cell nuclei and in glial cell nuclei. As far as the liver is concerned, at F14 the expression of TR isoforms was weaker in hepatocytes when, on the contrary, TR alpha was clearly detected in hematopoietic cells. The expression of TRs in hepatocytes becomes evident later. The data that we obtained, although not quantitative, emphasize the presence of each TR isoform in brain and liver from 14 days of fetal rat life.

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“…different from the control stained with normal rabbit serum. We have reported similar data obtained in adult rat heart utilizing the same antibodies for immunohistochemical analysis (26).…”

Section: Resultssupporting

confidence: 72%

Section: Methodsmentioning

confidence: 99%

Evaluation of the ontogeny of thyroid hormone receptor isotypes in rat brain and liver using an immunohistochemical technique

Falcone

Miyamoto²,

Fierro-Renoy³

et al. 1994

European Journal of Endocrinology

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“…It is well known that Thra and Thrb mRNAs are expressed in most rat tissues, although their relative abundance varies (Cheng et al 2010 for review). For example Thra1 is the major isoform expressed in the heart (Falcone et al 1992, Mai et al 2004, whereas Thrb1 predominates in the liver (Harvey & Williams 2002). In the brain, Thra1 is the major foetal isoform, but at birth, there is a marked increase in the expression of Thrb1, which is later maintained during adult life (Harvey & Williams 2002).…”

Section: Discussionmentioning

confidence: 99%

Triiodothyronine induces lipid oxidation and mitochondrial biogenesis in rat Harderian gland

Santillo

Burrone

Falvo

et al. 2013

Journal of Endocrinology

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The rat Harderian gland (HG) is an orbital gland producing a copious lipid secretion. Recent studies indicate that its secretory activity is regulated by thyroid hormones. In this study, we found that both isoforms of the thyroid hormone receptor (Tra (Thra) and Trb (Thrb)) are expressed in rat HGs. Although Thra is expressed at a higher level, only Thrb is regulated by triiodothyronine (T 3 ). Because T 3 induces an increase in lipid metabolism in rat HGs, we investigated the effects of an animal's thyroid state on the expression levels of carnitine palmitoyltransferase-1A (Cpt1a) and carnitine palmitoyltransferase-1B (Cpt1b) and acyl-CoA oxidase (Acox1) (rate-limiting enzymes in mitochondrial and peroxisomal fatty acid oxidation respectively), as well as on the mitochondrial compartment, thereby correlating mitochondrial activity and biogenesis with morphological analysis. We found that hypothyroidism decreased the expression of Cpt1b and Acox1 mRNA, whereas the administration of T 3 to hypothyroid rats increased transcript levels. Respiratory parameters and catalase protein levels provided further evidence that T 3 modulates mitochondrial and peroxisomal activities. Furthermore, in hypothyroid rat HGs, the mitochondrial number and their total area decreased with respect to the controls, whereas the average area of the individual mitochondrion did not change. However, the average area of the individual mitochondrion was reduced by w50% in hypothyroid T 3 -treated HGs, and the mitochondrial number and the total area of the mitochondrial compartment increased. The mitochondrial morphometric data correlated well with the molecular results. Indeed, hypothyroid status did not modify the expression of mitochondrial biogenesis genes such as Ppargc1a, Nrf1 and Tfam, whereas T 3 treatment increased the expression level of these genes.

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“…Because of the lack of this inhibition, circulating levels of TSH and TH are consequently elevated in the TR␤ PV/PV mutant. TR␣ is the dominant TH receptor in the heart, e.g., threefold higher than the TR␤ receptor (6), and is functionally normal in the TR␤ PV/PV mice. It may therefore be mediating the effects of the increased circulating TH to produce a thyrotoxic response in the heart, manifested by the increased heart rate previously observed in TR␤-deficient knockout mutant mice (13) and the Fig.…”

Section: Discussionmentioning

confidence: 99%

Cardiac glucose utilization in mice with mutated α- and β-thyroid hormone receptors

Esaki¹,

Suzuki²,

Cook³

et al. 2004

American Journal of Physiology-Endocrinology and Metabolism

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Abnormal thyroid function is usually associated with altered cardiac function. Mutations in the thyroid hormone (TH)-binding region of the TH beta-receptor (TRbeta) that eliminate its TH-binding ability lead to the thyroid hormone resistance syndrome (RTH) in humans, which is characterized by high blood TH levels, goiter, hyperactivity, and tachycardia. Mice with "knock-in" mutations in the TH alpha-receptor (TRalpha) or TRbeta that remove their TH-binding ability have been developed, and those with the mutated TRbeta (TRbeta(PV/PV)) appear to provide a model for RTH. These two types of mutants show different effects on cerebral energy metabolism, e.g., negligible change in glucose utilization (CMR(Glc)) in TRbeta(PV/PV) mice and markedly reduced CMR(Glc), like that found in cretinous rats, in the mice (TRalpha(PV/+)) with the knock-in mutation of the TRalpha gene. Studies in knockout mice have indicated that the TRalpha may also influence heart rate. Because mutations in both receptor genes appear to affect some parameters of cardiac function and because cardiac functional activity and energy metabolism are linked, we measured heart glucose utilization (HMR(Glc)) in both the TRbeta(PV/PV) and TRalpha(PV/+) mutants. Compared with values in normal wild-type mice, HMR(Glc) was reduced (-77 to -95%) in TRalpha(PV/+) mutants and increased (87 to 340%) in TRbeta(PV/PV) mutants, the degree depending on the region of the heart. Thus the TRalpha(PV/+) and TRbeta(PV/PV) mutations lead, respectively, to opposite effects on energy metabolism in the heart that are consistent with the bradycardia seen in hypothyroidism and the tachycardia associated with hyperthyroidism and RTH.

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Antipeptide polyclonal antibodies specifically recognize each human thyroid hormone receptor isoform.

Cited by 81 publications

References 29 publications

Evaluation of the ontogeny of thyroid hormone receptor isotypes in rat brain and liver using an immunohistochemical technique

Evaluation of the ontogeny of thyroid hormone receptor isotypes in rat brain and liver using an immunohistochemical technique

Triiodothyronine induces lipid oxidation and mitochondrial biogenesis in rat Harderian gland

Cardiac glucose utilization in mice with mutated α- and β-thyroid hormone receptors

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