Influence of a Ctsk-/-/Mct8-/y/Mct10-/- triple knockout on the tanscriptome of thyroid tissue in male mice
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ABSTRACT:
PROVIDER: PRJNA685136 | ENA |
REPOSITORIES: ENA
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Project description:To investigate the influence of cathepsin k and the monocarboxylate transporters 8 and 10 on the protein profile in thyroid tissue, we used a Ctsk-/-/Mct8-/y/Mct10-/- triple knockout mouse model and performed proteome analyses.
2020-12-14 | MSV000086595 | MassIVE
Project description:To investigate the influence of cathepsin k and the monocarboxylate transporters 8 and 10 on the gene expression profile in thyroid tissue, we used a Ctsk-/-/Mct8-/y/Mct10-/- triple knockout mouse model and performed microarray analyses.
2021-01-04 | GSE163168 | GEO
Project description:RNA sequencing (RNAseq) in testis tissue has been done to obtain an answer about the influence of Tcte1 null mutation in knockout mice on the expression pattern of other gonadal genes in male animals that may be influential for male fertility status. Homozygous males (infertile) revealed oligoasthenoteratozoospermia (incl. circular pathway of sperm motility), while heterozygous animals (fertile) manifested oligozoospermia, suggesting haploinsufficiency. RNA-sequencing of the mutant testicular tissue showed the influence of Tcte1 mutations on the expression pattern of genes responsible for mitochondrial ATP processing, linked with apoptosis, or spermatogenesis.
2023-02-01 | GSE207805 | GEO
Project description:Background: Sex and age have substantial influence on thyroid function. Sex influences the risk and clinical expression of thyroid disorders (TDs), with age a proposed trigger for the development of TDs. Cardiac function is affected by thyroid hormone levels with gender differences. Accordingly, we investigated the proteomic changes involved in sex based cardiac responses to thyroid dysfunction in elderly mice. Methods: Aged (18-20 months) male and female C57BL/6 mice were fed diets to create euthyroid, hypothyroid, or hyperthyroid states. Serial echocardiographs were performed to assess heart function. Proteomic changes in cardiac protein profiles were assessed by 2-D DIGE and LC-MS/MS, and a subset confirmed by immunoblotting. Results: Serial echocardiographs showed ventricular function remained unchanged regardless of treatment. Heart rate and size increased (hyperthyroid) or decreased (hypothyroid) independent of sex. Pairwise comparison between the six groups identified 55 proteins (≥ 1.5-fold difference and p < 0.1). Compared to same-sex controls 26/55 protein changes were in the female hypothyroid heart, whereas 15/55 protein changes were identified in the male hypothyroid, and male and female hyperthyroid heart. The proteins mapped to oxidative phosphorylation, tissue remodeling and inflammatory response pathways. Conclusion: We identified both predicted and novel proteins with gender specific differential expression in response to thyroid hormone status, providing a catalogue of proteins associated with thyroid dysfunction. Pursuit of these proteins and their involvement in cardiac function will expand our understanding of mechanisms involved in sex-based cardiac response to thyroid dysfunction.
2020-12-23 | PXD022557 | Pride
Project description:Aortic Effects of Thyroid Hormone in Male Mice
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Project description:In the present study, we examine expression profiles of normal tissue fragments, intraoperatively taken on the basis of macroscopic judgment and confirmed by immunohistochemistry, from patients with neoplastic and non-neoplastic disease of thyroid. The distinct GEP detected may influence the insurgence and/or progression of thyroid cancer, its molecular classification, and thus pinpoint selective gene targets for new preoperative diagnostic approaches treatments and prophylactic strategies.
2016-05-06 | E-MTAB-3796 | biostudies-arrayexpress
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
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
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.
2010-12-01 | GSE22118 | GEO
Project description:Test for thyroid hormone regulation of genes expressed in the abdominal aorta of C57Bl6 mice. Comparison between mice treated with 1mg/L Thyroxin in drinking water for 4 days compared to controls.
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