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A cardiac developmental defect prevents thyroid hormone induced tachycardia in Resistance to Thyroid Hormone alpha

ABSTRACT: A cardiac developmental defect prevents thyroid hormone induced tachycardia in Resistance to Thyroid Hormone alpha

PROVIDER: PRJNA850193 | ENA |

REPOSITORIES: ENA

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A cardiac developmental defect prevents thyroid hormone induced tachycardia in the syndrome of resistance to thyroid hormone alpha

Project description:A cardiac developmental defect prevents thyroid hormone induced tachycardia in the syndrome of resistance to thyroid hormone alpha

| PRJNA947171 | ENA

A cardiac developmental defect prevents thyroid hormone induced tachycardia in the syndrome of resistance to thyroid hormone alpha

Project description:A cardiac developmental defect prevents thyroid hormone induced tachycardia in the syndrome of resistance to thyroid hormone alpha

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A cardiac developmental defect prevents thyroid hormone induced tachycardia in Resistance to Thyroid Hormone alpha

Project description:Purpose: The objective of this study was to determine the cardiac gene expression prifile in the whole heart of mice with mutated thyroid receptor alpha 1 (TRα1R384C+/m) in control condition as well as after treatement with 3,3´,5-triiodo-L-thyronine (T3) for 12 days.

2023-04-23 | GSE206337 | GEO

A cardiac developmental defect prevents thyroid hormone induced tachycardia in the syndrome of resistance to thyroid hormone alpha

Project description:Purpose: the objective of this study was to determine cardiac gene expression profile in the mice heart of mutated thyroid receptor alpha 1 (TRα1R384C+/m) male offspring of control dams as well as of dams treated with 3,3',5-triiodo-L-thyronine (T3) from embryonic day 12.5 to 18.5

2023-04-23 | GSE227847 | GEO

A cardiac developmental defect prevents thyroid hormone induced tachycardia in the syndrome of resistance to thyroid hormone alpha

Project description:Purpose: the objective of this study was to determine the whole DNA methylation profile in the mice heart of mutated thyroid receptor alpha 1 (TRα1R384C+/m) male offspring of control dams as well as of dams treated with 3,3',5-triiodo-L-thyronine (T3) from embryonic day 12.5 to 18.5

2023-04-23 | GSE226701 | GEO

GLIS3 is indispensable for TSH/TSHR-dependent thyroid hormone biosynthesis and follicular cell proliferation

Project description:Deficiency in Krüppel-like zinc finger transcription factor, GLI-Similar 3 (GLIS3) in humans is associated with the development of congenital hypothyroidism. However, the functions of GLIS3 in the thyroid gland and by what mechanism GLIS3-dysfunction causes hypothyroidism are unknown. In this study, we demonstrate that GLIS3 acts downstream of thyroid stimulating hormone (TSH)/TSHR and is indispensable for TSH/TSHR-mediated induction of thyroid follicular cell proliferation and thyroid hormone biosynthesis. ChIP-Seq and promoter analysis revealed that GLIS3 is critical for the transcriptional activation of several genes required for thyroid hormone biosynthesis, including the iodide transporters Nis and Pds, indicating that these genes are directly regulated by GLIS3. The repression of cell proliferation regulatory genes is due to the inhibition of TSH-mediated activation of the mTORC1/RPS6 pathway as well as direct transcriptional regulation of several cell division-related genes by GLIS3. Consequently, GLIS3-deficiency prevents the development of goiter as well as the induction of inflammatory and fibrotic genes during chronic elevation of circulating TSH. Our study identifies GLIS3 as a new and key regulator of TSH/TSHR-mediated thyroid hormone biosynthesis and proliferation of thyroid follicular cells, and uncovers a mechanism by which GLIS3-deficiency causes congenital hypothyroidism and prevents goiter development.

2017-08-30 | GSE103297 | GEO

Thyroid hormone receptor beta is required for thyrotrpin regulation and thyroid hormone production.

Project description:Thyroid hormone receptor beta is required for thyrotrpin regulation and thyroid hormone production.

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Thyroid hormone receptor alpha is required for thyroid hormone-dependent neural cell proliferation during tadpole metamorphosis

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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.

2020-09-21 | GSE146336 | GEO

Target genes of thyroid hormone in cerebellum neurons

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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