Thyroid hormone-responsive genes in primary cultures of rat hepatic cells
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PROVIDER: PRJNA1189567 | ENA |
REPOSITORIES: ENA
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Project description:cDNA microarray analysis was applied to primary cultures of rat hepatic cells treated with triiodothyronine (T3) at 10-9 M for 24 hrs to identify the differentially expressed genes. A limited number of genes were listed, and only 3 of them, pyridoxal kinase (Pdxk), phosphoe-nolpyruvate carboxykinase 1 (Pck1), and solute carrier family 17 member 2 (Slc17a2), were con-firmed to be up-regulated by quantitative RT-PCR.
2024-11-27 | GSE282664 | GEO
Project description:Thyroid hormone-responsive miR-378 modulates cholesterol homeostasis by regulating hepatic bile acid synthesis
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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. Primary cultures of cerebellar neurons were made by dissociation of cerebella from newborn wild-type mice. These cells were plated 48 hours in serum-free medium to avoid invasion of the culture by glial cells. In order to include a kinetic and a maximum number of target genes, several cultures were either treated or left untreated as controls for 6 hours (T1), 16 hours (T2), 24 hours (T3) or 48 hours (T4) and results were pairwise compared for each time point.
2012-03-29 | E-GEOD-24793 | biostudies-arrayexpress
Project description:Tagged versions of thyroid hormone receptors alpha (TRa) and beta (TRb) were stably transfected in two C17.2 cell lines, C17.2a and C17.2b, respectively. Cells were treated with 10-7 M T3 for 6, 12 or 24h or left untreated. We performed DGE by sequencing all polyA RNA according to a SAGE-derived method. Differential gene expression after T3 treatment was computed and the T3 responses induced by the two receptors were compared. We could conclude that, in a similar environment, target genes are only partially shared and that a significant proportion show receptor preference and even selectivity. Examination of thyroid hormone target genes over time in two cell lines (C17.2a, C17.2b), each expressing one of the thyroid hormone receptors (alpha, beta).
2012-12-31 | E-GEOD-38539 | biostudies-arrayexpress
Project description:chip on chip to identify thyroid hormone receptor responsive gene
2009-04-03 | E-MEXP-1801 | biostudies-arrayexpress
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.
2025-08-22 | GSE305978 | GEO
Project description:Thyroid hormone receptor beta is required for thyrotrpin regulation and thyroid hormone production.
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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.
2025-08-11 | GSE304918 | GEO
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: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