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Thyroid hormone-responsive genes in primary cultures of rat hepatic cells

ABSTRACT: Thyroid hormone-responsive genes in primary cultures of rat hepatic cells

PROVIDER: PRJNA1189567 | ENA |

REPOSITORIES: ENA

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Thyroid hormone-responsive genes in primary cultures of rat hepatic cells

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.

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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. 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

Digital Gene Expression (DGE) of thyroid hormone (T3)-responsive genes in C17.2 cells stably transfected with thyroid hormone receptors alpha and beta

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).

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Thyroid hormone-responsive miR-378 modulates cholesterol homeostasis by regulating hepatic bile acid synthesis

Project description:An improved mechanistic understanding of the thyroid hormone (TH) action on bile acid (BA) synthetic pathway, the major route for cholesterol elimination, will facilitate the identification of novel therapeutic targets for hypercholesterolemia. Here, we show that hepatic miR-378 is positively regulated by TH. Transient overexpression of miR-378 in the liver of mice reduces the serum cholesterol levels, which is accompanied with an upregulation of key enzymes involved in the intrahepatic conversion of cholesterol to BAs. Importantly, transgenic mice with liver-specific and moderate overexpression of miR-378 also display a decrease in serum cholesterol levels accompanied with an enhanced BA synthesis and are resistant to diet-induced hypercholesterolemia. In contrast, mice lacking miR-378 exhibit an elevation of serum cholesterol levels accompanied with an impaired BA synthesis. Mechanistic studies reveal that hepatic miR-378 regulates BA synthesis and cholesterol homeostasis through its direct target gene MAFG, which is a transcriptional repressor of BA synthetic genes. We also show that miR-378 serves as an essential component in either incoherent or coherent feed-forward loop to confer robust and precise controls on BA synthesis in response to TH signalling. Together, we identify a previously undescribed miR-378-mediated mechanism underlying the cholesterol-lowering effect of TH. Our findings not only add a new dimension to our understanding the regulation of BA synthesis by TH, but also provide new therapeutic regimens to manage serum cholesterol levels

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Characterization of Directly Regulated Thyroid Hormone Mediated Gene Expression Following Short-Term Perturbations in Thyroid Hormone Levels in Juvenile Mice

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.

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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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