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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of rat thyroid cell lines after TSH-stimulation

ABSTRACT: A time-course analysis of TSH-stimulation in two rat thyroid cell lines (FRTL5 and FRT/TSHR) was performed. The expression levels of 8,784 transcripts were measured at three different time points, i.e. before (0), 30 minutes (30m) and 17 hours (17h) after TSH stimulation, by means of Affymetrix RG-U34A arrays. Experiment Overall Design: 2 cell lines, 3 time points and 3 biological replicates per time point were analyzed

ORGANISM(S): Rattus norvegicus

SUBMITTER: Davide Calebiro

PROVIDER: E-GEOD-5115 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Selective modulation of protein kinase A I and II reveals distinct roles in thyroid cell gene expression and growth.

Calebiro Davide D de Filippis Tiziana T Lucchi Simona S Martinez Fernando F Porazzi Patrizia P Trivellato Roberta R Locati Massimo M Beck-Peccoz Paolo P Persani Luca L

Molecular endocrinology (Baltimore, Md.) 20060803 12

A global gene expression profiling of TSH stimulation on differentiated (FRTL5) and partially dedifferentiated [FRT/TSHR (TSH receptor)] rat thyroid cells was performed. A total of 123 TSH-regulated genes (95 newly described) were identified in FRTL5, whereas no significant transcriptional modifications were seen in FRT/TSHR cells. Because regulatory subunit IIbeta (RIIbeta) of protein kinase A (PKA), a key element downstream of cAMP, was expressed in FRTL5 but not in cAMP-refractory FRT/TSHR ce ...[more]

PMID: 16887886

Similar Datasets

Time course analysis of TSH-stimulated rat thyroid cell lines

Project description:A time-course analysis of TSH-stimulation in two rat thyroid cell lines (FRTL5 and FRT/TSHR) was performed. The expression levels of 8,784 transcripts were measured at three different time points, i.e. before (0), 30 minutes (30m) and 17 hours (17h) after TSH stimulation, by means of Affymetrix RG-U34A arrays. Keywords: Time course

2006-10-01 | GSE5115 | GEO

Effect of iodine on early stage thyroid autonomy

Project description:Thyroid autonomy is a frequent cause of thyrotoxicosis in regions with iodine deficiency. Epidemiological data suggest that the prevalence of thyroid autonomy is not only inversely correlated with the ambient iodine supply, but that iodide may also influence the course of pre-existing thyroid autonomy with possibly different effects on thyroid growth and function. Iodine slows TSH effects on thyroid growth stimulation and this effect is more pronounced in thyrocytes with constitutive cAMP activation i.e. in thyroid autonomy. Iodine induced growth alteration in early stage thyroid autonomy is conferred by induction of apoptosis and G2/M arrest. Transcriptome analysis revealed significant modulation of gene networks relevant to cell adhesion, cadherin signalling and ion binding with more pronounced effects in constitutively active FRTL-5 cells compared to normal FRTL-5 cells. The aim was to study iodide-induced changes in global gene expression in an in vitro model of thyroid autonomy. This model makes use of FRTL-5 cells with stable expression of a constitutively activating TSH receptor mutation or wild type TSHR as a control.

2010-12-01 | E-GEOD-22118 | biostudies-arrayexpress

Thyrotropin Receptor Signaling Deficiency Impairs Spatial Learning and Memory

Project description:Subclinical hyperthyroidism, a disease characterized by decreased thyroid-stimulating hormone (TSH) and normal concentration of thyroid hormone, is associated with an elevated risk for cognitive impairment. TSH is the major endogenous ligand of TSH receptor (TSHR) and its role dependent on the process of signal transduction of TSHR. It has not, however, been established whether TSHR signaling are involved in the regulation of cognition. In the current study, Tshr deletion leads to significantly compromised performance in hippocampus-dependent tasks, along with reduced dendritic spine density and excitatory synaptic density as well as altered synaptic structure in CA1 subfield of the hippocampus. Furthermore, the synapse-related gene expression was altered in the hippocampus of Tshr-/- mice. These findings suggest the ablation of TSHR signaling impairs spatial learning and memory, which reveals a fresh role of TSHR signaling in brain.

2022-02-28 | GSE145958 | GEO

RhoA inhibitor treatment of spinal cord injury: Deep inside mechanism understanding for a better use

Project description:The present study shows by in vivo experiments, the impact of RhoA inhibitor treatment using a functionalized alginate scaffold and the beneficial results at the early stage by increasing neurites outgrowth and synaptic contact. However, 7 days after treatment a plateau is obtained in BBB score. We thus performed an in vitro and proteomic associated to systemic biology analyses of secreted factors from ND7/23 DRG cell line incubated with secreted factors from different segments after spinal cord lesion treated wih RhoA inhibitor. We then performed a time course proteomic study from the DRG cells in same conditions as for the secretome. The results taken together allow a better understanding of the mechanisms occurring in both side of the lesion and led a positive impact of the treatment on growth cone guidance in both sides of the lesion (Rostral 1 and Caudal 1). We identified the transcription factors involved in time course at the beginning of the treatment and the growth cone factors (receptors, ligands, signaling pathways) implicated in this time course. We also demonstrate the involvement of immunoglobulins (IgG1, IgG2) in this process. Anti-GFAP seem to bind to its own receptor in DRG cells when neurite outgrowth is initiated and thus modulate the process like in traumatic brain injury. These results open the door of a concomitant treatment at both sides of the lesion with RhoA inhibitor. However, we also pointed that RhoA inhibitor treatment led to an inhibition of several factors implicated in neurogenesis reflecting a global inhibition at term as detected in vivo that reached 2 weeks after treatment. RhoA inhibitor treatment is useful to initiate the neurogenesis process but needs to be supplied by a second treatment for increasing synaptic connections and the neuron reconnections.

2017-07-28 | PXD004639 | Pride

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

Gene expression profile of TGFβ3 stimulation and TRPV4 activation/inhibition in the TC28a2 human chondrocyte cell line

Project description:RNA-seq of TC28a2 cells following TRPV4 activation/inhibition in the presence and absence of prior TGFβ3 stimulation. The experiment was performed to determine the effect of TRPV4 activity on gene expression in the presence and absence of TGFβ stimulation. TGFβ3 was used to stimulate TGFβ signalling, GSK1016790A (GSK101) was used to activate TRPV4, GSK2193874 (GSK219) was used to inhibit TRPV4 and DMSO was used as a vehicle control.

2022-01-17 | E-MTAB-10279 | biostudies-arrayexpress

Effect of simultaneous activation of TGFbeta and TLR4 pathway in human monocytes

Project description:To better understand the interaction of TGFbeta and Toll-like-receptor 4 (TLR4) signaling in monocytes, we performed microarray analysis. We identified a unique set of genes whose expressions in monocytes were regulated by simultaneous stimulation of TLR4 and TGFβ signaling. THP-1 cells, a human monocytic cell line, were stimulated for 24 hours with PBS as control, LPS (100ng/ml), TGFbeta1 (1ng/ml) or LPS (100ng/ml) + TGFbeta1 (1ng/ml). After 24 hours of stimulation, total RNA was isolated and prepared for genome wide analyses using Illumina HumanRef8 V3.0 Beadchips. In total 32 arrays were analyzed including 8 samples of PBS-stimulated monocytes, 8 samples of LPS-stimulated monocytes, 8 samples of TGFbeta1 stimulated monocytes and 8 samples of monocytes stimulated with LPS + TGFbeta1.

2012-12-15 | E-GEOD-17909 | biostudies-arrayexpress

Proteome of mouse primary CD4 T cells

Project description:We analyzed the total proteome of CD4+ T cells isolated from WT mice, either non stimulated or at 5 different time points of stimulation with anti-CD3 and anti-CD4 antibodies (30s; 120s; 300s; 600s)

2019-09-27 | PXD012826 | Pride

Transcription profiling of mouse NIH3T3 cell line cultured with and withput FGF and treated with the MEK Inhibitor U0126 at 3 time points before FGF addition reveals ERK-dependent downregulated genes have the ability to block S phase entry

Project description:The ERK family of MAP kinase plays a critical role in growth factor-stimulated cell cycle progression from G0/G1 to S phase. But, how sustained activation of ERK promotes G1 progression has remained unclear. Here, our systematic analysis on the temporal program of ERK-dependent gene expression shows that sustained activation of ERK is required for induction and maintenance of the decreased expression levels of a set of genes. Moreover, our cell biological analysis reveals that these ERK-dependent downregulated genes have the ability to block S phase entry. Cessation of ERK activation at mid or late G1 leads to a rapid increase of these anti-proliferative genes and results in the inhibition of S phase entry. These findings uncover an important mechanism by which the duration of ERK activation regulates cell cycle progression through dynamic changes in gene expression, and identify novel ERK target genes crucial for the regulation of cell cycle progression.

2007-11-24 | E-GEOD-4739 | biostudies-arrayexpress

Human-derived PBMCs were stimulated by different groups to kill tumor cells.After 48 hours, PBMCs were taken out, and the enrichment of activated proteins of relevant lymphocytes and the regulation of pathways were examined by proteomics.

Project description:In this study, proteomics was used to explore the activation of lymphocytes and related pathways in PBMCs of different stimulation groups. In our study, proteomics analysis showed that the immune cells in PBMCs activated by stimulation group exhibit improved functions related to white blood cell activation, proliferation and cytotoxicity during biological processes. At the same time, KEGG pathway analysis showed that the signaling pathways’ key proteins for leukocyte transendothelial migration, Th1/Th2 cell differentiation, JAK-STAT (involved in many important biological processes such as cell proliferation, differentiation, apoptosis and immune regulation), DNA replication and Th17 cell differentiation were up-regulated; whereas the key proteins of necroptosis pathways in immune cells were down-regulated.

2023-07-20 | PXD026739 | Pride

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