The thyroid hormone receptors regulate the expression of microRNAs with key roles in skin homeostasis
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE107065 | GEO | 2018/06/08
REPOSITORIES: GEO
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Project description:An excess in thyroid hormone during rodent neonatal life causes abnormal prolifration and maturation of testicular cells, leading to reduced testis size and impairments in steroidogenesis, Sertoli cell function, spermatogenesis and fertility. The high expression of type 3 deiodinase in the neonatal testis protects this tissue from premature exposure to thyroid hormones, since this gene (Dio3) function is to degrade thyroid hormones. DIO3-deficient mice (Dio3KO) exhibit a marked reduction in Sertoli cell proliferation and testis size, abnormalities in the reproductive axis and impaired fertility (Martinez et al. 2016, Endocrinology157:1276). To identify genes that are untimely regulated by thyroid hormone in the developing testes, we have performed RNAseq in testis total RNA from wild type and DIO3KO mouse neonates.
2019-08-01 | GSE117157 | GEO
Project description:The thyroid hormone receptors regulate the expression of microRNAs with key roles in skin homeostasis
| PRJNA418948 | ENA
Project description:Thyroid hormone receptors (TRs) are hormone-regulated transcription factors that control multiple aspects of physiology and development. TRs are expressed in vertebrates as a series of distinct isoforms that exert distinct biological roles. We wished to determine if the two most widely expressed isoforms, TRa1 and TRb1, exert their different biological effects by regulating different sets of target genes. Using stably transformed HepG2 cells and a microarray analysis, we were able to demonstrate that TRa1 and TRb1 regulate a largely overlapping repertoire of target genes in response to T3 hormone. However, these two isoforms display very different transcriptional properties on each individual target gene, ranging from a much greater T3-mediated regulation by TRa1 than by TRb1, to near equal regulation by both isoforms. We also identified TRa1 and TRb1 target genes that were regulated by these receptors in a hormone-independent fashion. We suggest that it is this gene-specific, isoform-specific amplitude of transcriptional regulation that is the likely basis for the appearance and maintenance of TRa1 and TRb1 over evolutionary time. In essence, TRa1 and TRb1 adjust the magnitude of the transcriptional response at different target genes to different levels; by altering the ratio of these isoforms in different tissues or at different developmental times, the intensity of T3 response can be individually tailored to different physiological and developmental requirements. TRa1, TRb1, or empty plasmid control stably transfected HepG2 cells were treated with 100 nM T3 or with ethanol carrier alone for 6h. Three independent biological repeats were analyzed for each of the three transformant pools (empty plasmid control, TRa1, and TRb1).
2009-08-08 | E-GEOD-17561 | biostudies-arrayexpress
Project description:Notch signaling between neighboring cells vitally contributes to specifying their identity and function, during development and in the adult. Here, we demonstrate that selective blockade of the Notch ligands JAG1 and JAG2 disrupts thermoregulation in adults by decreasing circulating thyroid hormones and thyroid function. Sequencing data in BAT demonstrates that Notch inhibition increases thermoregulation genes and this depends on thyroid hormones.
2023-10-23 | GSE200266 | GEO
Project description:We examined the impact of thyroid hormone excess on the mouse fetal heart utilizing a model of deficiency in DIO3, the enzyme that is responsible for clearing thyroid hormones
2022-11-23 | GSE198416 | GEO
Project description:Thyroid hormone receptors (TRs) are hormone-regulated transcription factors that regulate a diverse array of biological activities, including metabolism, homeostasis, and development. TRs also serve as tumor suppressors, and aberrant TR function (via mutation, deletion, or altered expression) is associated with a spectrum of both neoplastic and endocrine diseases. A particularly high frequency of TR mutations has been reported in renal clear cell carcinoma (RCCC) and in hepatocellular carcinoma (HCC). We have shown that HCC-TR mutants regulate only a fraction of the genes targeted by wild-type TRs, but have gained the ability to regulate other, unique, targets. We have suggested that this altered gene recognition may contribute to the neoplastic phenotype. Here, to determine the generality of this phenomenon, we examined a distinct set of TR mutants associated with RCCCs. We report that two different TR mutants, isolated from independent RCCC tumors, possess greatly expanded target gene specificities that extensively overlap one another, but only minimally overlap that of the WT-TRs, or those of two HCC-TR mutants. Many of the genes targeted by either or both RCCC-TR mutants have been previously implicated in RCCC, and include a series of metallothioneins, solute carriers, and genes involved in glycolysis and energy metabolism. We propose that TR mutations from RCCC and HCC are likely to play tissue-specific roles in carcinogenesis, and that the divergent target gene recognition patterns of TR mutants isolated from the two different types of tumors arises from different selective pressures during development of RCCC versus HCC. Gene expression was analyzed in HepG2 transformants expressing ectopic wildtype THRA, wildtype THRB, HCC-TR mutants ?? and ?N, and RCCC-TR mutants 6? and 15? using Affymetrix Human Gene 1.0 ST arrays in the presence or absence of T3. Each HepG2 transformant was assayed in triplicate.
2011-05-10 | E-GEOD-29159 | biostudies-arrayexpress
Project description:Notch signaling between neighboring cells vitally contributes to specifying their identity and function, during development and in the adult. Here, we demonstrate that selective blockade of the Notch ligands JAG1 and JAG2 disrupts thermoregulation in adults by decreasing circulating thyroid hormones and thyroid function. By exploiting single-cell methods to carefully evaluate the thyroid, an understudied apex endocrine organ, we discovered unexpected thyrocyte heterogeneity, marked by three distinct thyrocyte subtypes with different Notch activation patterns.
2023-10-23 | GSE200267 | GEO
Project description:Notch signaling between neighboring cells vitally contributes to specifying their identity and function, during development and in the adult. Here, we demonstrate that selective blockade of the Notch ligands JAG1 and JAG2 disrupts thermoregulation in adults by decreasing circulating thyroid hormones and thyroid function. Sequencing data demonstrates that Notch inhibition decreases thyrocyte markers and mitochondrial genes.
2023-10-23 | GSE200265 | GEO
Project description:Thyroid hormone receptors (TRs) are hormone-regulated transcription factors that control multiple aspects of physiology and development. TRs are expressed in vertebrates as a series of distinct isoforms that exert distinct biological roles. We wished to determine if the two most widely expressed isoforms, TRa1 and TRb1, exert their different biological effects by regulating different sets of target genes. Using stably transformed HepG2 cells and a microarray analysis, we were able to demonstrate that TRa1 and TRb1 regulate a largely overlapping repertoire of target genes in response to T3 hormone. However, these two isoforms display very different transcriptional properties on each individual target gene, ranging from a much greater T3-mediated regulation by TRa1 than by TRb1, to near equal regulation by both isoforms. We also identified TRa1 and TRb1 target genes that were regulated by these receptors in a hormone-independent fashion. We suggest that it is this gene-specific, isoform-specific amplitude of transcriptional regulation that is the likely basis for the appearance and maintenance of TRa1 and TRb1 over evolutionary time. In essence, TRa1 and TRb1 adjust the magnitude of the transcriptional response at different target genes to different levels; by altering the ratio of these isoforms in different tissues or at different developmental times, the intensity of T3 response can be individually tailored to different physiological and developmental requirements.
2009-08-08 | GSE17561 | GEO
Project description:We investigated the effects of thyroid hormone disruptions on gene expression in juvenile mice liver to develop a stronger understanding of the mechanisms by which thyroid disrupting chemicals impair development. Gene expression was examined by hybridization of hepatic RNA to Agilent mouse microarrays for hyper-, hypo-, hypo-replacement (hypo+) and euthyroid animals. Keywords: Toxicogenomics, biomarkers of thyroid disruptors Hypothyroidism was induced from post natal day (PND) 13 to 15 by adding model thyroid toxicants methimazole and sodium perchlorate to drinking water of pregnant females. Hyperthyroidism was induced by intraperitoneal injections (i.p.) of THs at PND 15, 4 hours before decapitation and tissue collection. For the hypothyroid/replacement group; dams were provided with drinking water for 3 days (PND 13 to 15), containing a mixture of methimazole/sodium perchlorate. Pups then received intraperitoneal injections of thyoid hormones on PND 15, 4 hours before decapitation and tissue collection.
2012-03-29 | E-GEOD-21307 | biostudies-arrayexpress