Physiologic and biochemical actions of thyroid hormone

Schwartz, Harold L.; Oppenheimer, Jack H.

doi:10.1016/s0306-039x(78)80002-6

Cited by 23 publications

(14 citation statements)

References 149 publications

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“…That T3 increases the activity of biosynthetic pathways is not unexpected. The role of T3 in amino acid incorporation and biosynthesis of DNA and protein constituents has been well studied (reviewed by Schwartz and Oppenheimer [52]). T3 has also been shown to increase protein turnover in both cardiac and skeletal muscle (1,10,11).…”

Section: Resultsmentioning

confidence: 99%

Silencing of Wnt Signaling and Activation of Multiple Metabolic Pathways in Response to Thyroid Hormone-Stimulated Cell Proliferation

Miller

Park

Guo

et al. 2001

Molecular and Cellular Biology

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To investigate the transcriptional program underlying thyroid hormone (T3)-induced cell proliferation, cDNA microarrays were used to survey the temporal expression profiles of 4,400 genes. Of 358 responsive genes identified, 88% had not previously been reported to be transcriptionally or functionally modulated by T3. Partitioning the genes into functional classes revealed the activation of multiple pathways, including glucose metabolism, biosynthesis, transcriptional regulation, protein degradation, and detoxification in T3-induced cell proliferation. Clustering the genes by temporal expression patterns provided further insight into the dynamics of T3 response pathways. Of particular significance was the finding that T3 rapidly repressed the expression of key regulators of the Wnt signaling pathway and suppressed the transcriptional downstream elements of the ␤-catenin-T-cell factor complex. This was confirmed biochemically, as ␤-catenin protein levels also decreased, leading to a decrease in the transcriptional activity of a ␤-catenin-responsive promoter. These results indicate that T3-induced cell proliferation is accompanied by a complex coordinated transcriptional reprogramming of many genes in different pathways and that early silencing of the Wnt pathway may be critical to this event.Thyroid hormone (3,3Ј,5-triiodo-L-thyronine [T3]) receptors (TRs) are ligand-dependent transcription factors which are members of the steroid hormone/retinoic acid (RA) receptor superfamily. Two TR genes, TR␣ and TR␤, located on chromosomes 17 and 3, respectively, give rise, by alternative splicing, to three T3-binding TR isoforms, ␣1, ␤1, and ␤2 (reviewed by Cheng [12]). TRs mediate the biological activities of T3 by binding to specific DNA sequences known as the T3 response elements present in the promoter regions of T3 target genes (reviewed by Cheng [12]). The transcriptional regulatory activity of TRs depends not only on T3 and the types of T3 response elements but also on a host of coregulatory proteins, including corepressors, coactivators, and the tumor suppressor p53 (3, 38).The growth-stimulatory effect of T3 has long been recognized. In humans, lack of T3 during development leads to growth retardation and cretinism. Growth retardation is also evident in patients with resistance to T3, a genetic disease due to mutations in the TR␤ gene (54). TR␤1 mutants act in a dominant negative fashion to cause growth retardation and delayed bone maturation (54). Moreover, mutant mice harboring a potent dominant negative mutant TR␤1 also exhibit a similar phenotype (25,60).GC is a rat pituitary cell line that expresses functional TRs and has long been used as a model cell line to understand the mechanisms of T3 action. Previously we have shown that GC cells are induced to proliferate by T3 in cultured medium containing 10% T3-depleted (Td) serum (2, 27). This induction is T3 specific, because the inactive T3 analogs, L-thyronine and reverse T3, failed to stimulate proliferation of GC cells in the same culture medium (27). Recently...

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Section: Resultsmentioning

confidence: 99%

Silencing of Wnt Signaling and Activation of Multiple Metabolic Pathways in Response to Thyroid Hormone-Stimulated Cell Proliferation

Miller

Park

Guo

et al. 2001

Molecular and Cellular Biology

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“…Proposed mechanisms of this include reduction of fatty acid and carbohydrate metabolism leading to diminished production of ATP [10,11]. Deposits of mucopolysaccharide in peripheral nerves and metabolic disorders of Schwann cells may contribute to peripheral nerve compression and dysfunction in hypothyroid patients [12].…”

Section: Discussionmentioning

confidence: 99%

The effects of hypothyroidism on strength–duration properties of peripheral nerve

Yerdelen

Ertorer

Koç

2010

Journal of the Neurological Sciences

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“…This process could be accentuated by thyroid hormone, which has been shown to increase hydroxyl radical and superoxide generation in mitochondria (Marzoez et al, 1982;Fernandez et al, 1985;Maddaiah, 1990) and white blood cells (Videla et al, 1993) as well as decrease cellular (Fernandez et al, 1991) and mitochondrial (Maddaiah, 1990) GSH. As thyroid hormone has been shown to increase the incidence of PHS mortality (Buys et al, 1993) and is requisite for rapid growth (Schwartz and Oppenheimer, 1978), a major selection criterion in broiler breeding, stimulation of reactive oxygen species production and compromised antioxidant function mediated by thyroid hormone, could be key biochemical events in the etiology of PHS.…”

Section: Discussionmentioning

confidence: 99%

Effect of α-Tocopherol on Antioxidants, Lipid Peroxidation, and the Incidence of Pulmonary Hypertension Syndrome (Ascites) in Broilers

et al. 1995

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Research has demonstrated a compromised antioxidant capacity in broilers with pulmonary hypertension syndrome (PHS). Thus, the objective of the present study was to assess the effects of vitamin E on PHS-induced mortality, tissue antioxidants, and plasma lipid peroxides in male broilers. Control broilers were provided normal ventilation but others, maintained under low ventilation conditions to induce PHS, were randomly assigned to nonimplanted (NI), placebo (PL), or vitamin E (VE) implanted groups. The VE implant released a total of 15 mg of alpha-tocopherol from 0 to 3 wk of age. Tissues and blood samples were obtained at 3 and 5 wk of age from birds with (PHS+) and without (PHS-) PHS. Five-week PHS cumulative mortality was lowered by alpha-tocopherol with mortality rates of 3.6, 4.2, 11.9, and 11.8%, for Controls, VE, NI, and PL groups, respectively. The PHS+ birds exhibited lower body weights, higher hematocrit, right ventricular hypertrophy, lower alpha-tocopherol and glutathione (GSH) concentrations in liver and lung, as well as indicators of oxidative stress, including elevated plasma lipid peroxides and lower oxidized GSH in liver and erythrocytes, at 5 wk of age. All birds exhibited lower erythrocyte catalase activity at 5 than at 3 wk of age. An improved antioxidant capacity was observed in VE birds, including higher liver and lung alpha-tocopherol at 3 and 5 wk, higher liver GSH at 3 wk, and lower plasma lipid peroxide values at 5 wk of age. Direct correlations observed between body weight and plasma lipid peroxides at 3 wk (r = .45) and between right ventricular hypertrophy and plasma lipid peroxides at 5 wk (r = .48), suggests that lipid peroxidation plays a role in the etiology of PHS. The results indicate that the VE implant was effective in lowering PHS-induced mortality in broilers apparently by attenuating processes leading to lipid peroxidation.

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Physiologic and biochemical actions of thyroid hormone

Cited by 23 publications

References 149 publications

Silencing of Wnt Signaling and Activation of Multiple Metabolic Pathways in Response to Thyroid Hormone-Stimulated Cell Proliferation

Silencing of Wnt Signaling and Activation of Multiple Metabolic Pathways in Response to Thyroid Hormone-Stimulated Cell Proliferation

The effects of hypothyroidism on strength–duration properties of peripheral nerve

Effect of α-Tocopherol on Antioxidants, Lipid Peroxidation, and the Incidence of Pulmonary Hypertension Syndrome (Ascites) in Broilers

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