Thyroid hormone receptor a in skeletal muscle is essential for thyroid thermogenesis
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ABSTRACT:
PROVIDER: PRJNA610173 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11234958_1.fastq.gz | Fastqsanger.gz | |||
| SRR11234958_2.fastq.gz | Fastqsanger.gz | |||
| SRR11234959_1.fastq.gz | Fastqsanger.gz | |||
| SRR11234959_2.fastq.gz | Fastqsanger.gz | |||
| SRR11234960_1.fastq.gz | Fastqsanger.gz |
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Project description:Thyroid hormones are important for homeostatic control of energy metabolism and body temperature. Although skeletal muscle is considered an important site for thyroid action, the contribution of thyroid hormone receptor signaling, in muscle, to whole-body energy metabolism and body temperature has not been resolved. Here, we show that thyroid hormone-induced increase in energy expenditure requires thyroid hormone receptor alpha 1 (TRa1) in skeletal muscle, but that thyroid hormone induced elevation in body temperature is independent of muscle-TRa1. In slow-twitch soleus muscle, ablation of TRa1 leads to an altered fiber type composition toward a more oxidative phenotype, which, however, does not influence running capacity or motivation to voluntary running. RNA-sequencing of soleus muscle from WT mice and TRaHSACre mice revealed differentiated transcriptional regulation of genes associated with muscle thermogenesis, such as sarcolipin and UCP3, thus providing molecular clues pertaining to the mechanistic underpinnings of TRa1-linked control of whole-body metabolic rate. Together, this work establishes a fundamental role for skeletal muscle in thyroid hormone-stimulated increase in whole-body energy expenditure.
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Project description:Metabolomics dataset of serum from T3-treated dams. Related to following publication by Oelkrug et al: "Maternal thyroid hormone receptor beta activation sparks brown fat thermogenesis in the offspring"
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Project description:In the current situation of the aging of the global population, primary sarcopenia is gradually attracting attention because of its potential risk to the elderly, high occult incidence and serious prognosis. As one of the most important hormones affecting skeletal muscle, the aging changes of thyroid hormone have been proved to be closely related to sarcopenia. Thyroid hormone exerts its effects locally in skeletal muscle by binding to thyroid hormone receptor. TRα is the main distribution type of thyroid hormone receptor in skeletal muscle. We have previously found the potential role of TRα in the aging process of skeletal muscle. As a nuclear transcription factor, TRα exerts subsequent biological effects by targeting regulatory genes. However, in the process of skeletal muscle aging, the target regulation map of TRα is still unclear.In this study, we constructed natural aging mouse models of different ages, combined ChIP-seq and mRNA-seq to explore the aging changes of TRα targets in skeletal muscle.
2025-06-03 | GSE281839 | GEO
Project description:In the current situation of the aging of the global population, primary sarcopenia is gradually attracting attention because of its potential risk to the elderly, high occult incidence and serious prognosis. As one of the most important hormones affecting skeletal muscle, the aging changes of thyroid hormone have been proved to be closely related to sarcopenia. Thyroid hormone exerts its effects locally in skeletal muscle by binding to thyroid hormone receptor. TRα is the main distribution type of thyroid hormone receptor in skeletal muscle. We have previously found the potential role of TRα in the aging process of skeletal muscle. As a nuclear transcription factor, TRα exerts subsequent biological effects by targeting regulatory genes. However, in the process of skeletal muscle aging, the target regulation map of TRα is still unclear.In this study, we constructed natural aging mouse models of different ages, combined ChIP-seq and mRNA-seq to explore the aging changes of TRα targets in skeletal muscle.
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Project description:This SuperSeries is composed of the following subset Series: GSE3461: Gene expression in miscellaneous human tissues and cell lines GSE3462: Triiodothyronine Treatment: Effects on vastus lateralis skeletal muscle Abstract: Thyroid hormones are key regulators of metabolism that modulate transcription via nuclear receptors. Hyperthyroidism is associated with increased metabolic rate, protein breakdown, and weight loss. Although the molecular actions of thyroid hormones have been studied thoroughly, their pleiotropic effects are mediated by complex changes in expression of an unknown number of target genes. Here, we measured patterns of skeletal muscle gene expression in five healthy men treated for 14 days with 75 µg of triiodothyronine, using 24,000 cDNA element microarrays. To analyze the data, we used a new statistical method that identifies significant changes in expression and estimates the false discovery rate. The 381 up-regulated genes were involved in a wide range of cellular functions including transcriptional control, mRNA maturation, protein turnover, signal transduction, cellular trafficking, and energy metabolism. Only two genes were down-regulated. Most of the genes are novel targets of thyroid hormone. Cluster analysis of triiodothyronine-regulated gene expression among 19 different human tissues or cell lines revealed sets of coregulated genes that serve similar biologic functions. These results define molecular signatures that help to understand the physiology and pathophysiology of thyroid hormone action. Refer to individual Series
2006-03-06 | E-GEOD-4345 | biostudies-arrayexpress
Project description:Abstract: Thyroid hormones are key regulators of metabolism that modulate transcription via nuclear receptors. Hyperthyroidism is associated with increased metabolic rate, protein breakdown, and weight loss. Although the molecular actions of thyroid hormones have been studied thoroughly, their pleiotropic effects are mediated by complex changes in expression of an unknown number of target genes. Here, we measured patterns of skeletal muscle gene expression in five healthy men treated for 14 days with 75 µg of triiodothyronine, using 24,000 cDNA element microarrays. To analyze the data, we used a new statistical method that identifies significant changes in expression and estimates the false discovery rate. The 381 up-regulated genes were involved in a wide range of cellular functions including transcriptional control, mRNA maturation, protein turnover, signal transduction, cellular trafficking, and energy metabolism. Only two genes were down-regulated. Most of the genes are novel targets of thyroid hormone. Cluster analysis of triiodothyronine-regulated gene expression among 19 different human tissues or cell lines revealed sets of coregulated genes that serve similar biologic functions. These results define molecular signatures that help to understand the physiology and pathophysiology of thyroid hormone action. This SuperSeries is composed of the SubSeries listed below.
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Project description:Thyroid hormone receptor beta is required for thyrotrpin regulation and thyroid hormone production.
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Project description:Using tadpoles mutant for thyroid hormone receptor alpha (thra), we show that TRa is required for thyroid hormone (T3) induction of cell proliferation in the brain. RNA-sequencing showed that the TRa is required for 95% of the gene regulation responses to T3.
2019-05-13 | GSE130816 | GEO
Project description:Maternal low thyroxine (T4) serum levels during the first trimester of pregnancy correlate with cerebral cortex volume and mental development of the progeny, but why neural cells during early fetal brain development are vulnerable to maternal T4 levels remains unknown. In this study, using iPSCs obtained from a boy with a loss-of-function mutation in MCT8—a transporter previously identified as critical for thyroid hormone uptake and action in neural cells—we demonstrate that thyroid hormones induce transcriptional changes that promote the progression of human neural precursor cells along the dorsal projection trajectory. Consistent with these findings, single-cell, spatial, and bulk transcriptomics from MCT8-deficient cerebral organoids and cultures of human neural precursor cells underscore the necessity for optimal thyroid hormone levels for these cells to differentiate into neurons. The controlled intracellular activation of T4 signaling occurs through the transient expression of the enzyme type 2 deiodinase, which converts T4 into its active form, T3, alongside the coordinated expression of thyroid hormone nuclear receptors. The intracellular activation of T4 in NPCs results in transcriptional changes important for their division mode and cell cycle progression. Thus, T4 is essential for fetal neurogenesis, highlighting the importance of adequate treatment for mothers with hypothyroidism.
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Project description:Cerebellar post-natal development is particularly sensitive to thyroid hormone and low levels of thyroid hormone (hypothyroidism) result in permanent defects in cerebellar architecture and function. All cell types of the cerebellum are affected, but the main sign of hypothyroidism in mice is the persistence of the external granular layer, composed of mitotic neuronal precursors at P21. To make the genetic link between thyroid hormone and cerebellar development, we sought to identify new thyroid hormone target genes, in particular in granule cells which represent the vast majority of cerebellar cells.
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