Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA304294 | ENA |
REPOSITORIES: ENA
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Project description:The role of unliganded thyroid hormone receptors (TRs) in human adipose derived stem cells (hADSC)
| PRJNA305074 | ENA
Project description:The goal of our present work was to understand the influence parvovirus B19 infection may have on the thyroid hormone signaling pathway, as well as the nuclear receptors (NR) pathway overall. We demonstrated that B19 infection of CD36+ erythroid progenitor cells leads to downregulation of the thyroid hormone receptor α isoform. In addition to that we have shown that B19 infection modulates the expression of other members of the NR superfamily such as estrogen and retinoid receptors. CD36+ cells (StemCell Technologies) were mock-infected or infected with B19, 48 hours post infection cells were collected, total RNA was isolated, and cDNA was obtained as described above. TaqMan® array human nuclear receptors fast 96-well plates obtained from Applied Biosystems (Carlsbad, CA) were utilized in order to assess the differences of 92 nuclear receptors’ expression in mock- and B19-infected CD36+ cells. Relative quantity (RQ) values were calculated using the 2-ΔΔCt method.
2012-11-04 | E-GEOD-42005 | biostudies-arrayexpress
Project description:To investigate the effect of thyroid hormone and its receptor on glucose and lipid metabolism in white adipose tissue (WAT), and the effect of thyroid hormone and its receptor on WAT regulation on glucose metabolism and obesity. We constructed mice with adipose tissue-specific knockout of thyroid hormone receptor beta（ATRβKO mice）. ATRβKO mice were given T3 stimulation or high-fat feeding. We then performed gene expression profiling analysis using data obtained from RNA-seq of White adipose tissue from knockout ATRβKO mice treated with T3 or HFD feeding.
2025-06-06 | GSE205520 | GEO
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: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. We performed an affinity-based purification of chromatin (ChAP), and high-throughput sequencing was used to assess binding sites of both receptors (ChAP-Seq). Standard ChIP-Seq for RXR was also performed in C17.2a cells. These data allow us to compare binding sites for both receptors and to conclude that they were only partially redundant, with co-existence of receptor-specific sites. Examination of binding sites of the two thyroid hormone receptors (alpha, beta) in two cell lines (C17.2a, C17.2b), each expressing one of the receptors. Examination of RXR binding sites in C17.2a cells.
2012-12-31 | E-GEOD-38347 | biostudies-arrayexpress
Project description:Effectively managing skin wounds to achieve quick and scarless healing is a significant clinical challenge. Several cell types participate in wound healing, including keratinocytes, fibroblasts, and many others. Human adipose-derived mesenchymal stem cell-derived exosomes (hADSC-Exos) are regarded as promising therapeutic choice. However, a comprehensive understanding of what mechanisms promote regenerative healing respond to hADSC-Exos treatment is still limited. Here, we utilize a high-resolution single-cell RNA sequencing analysis (scRNA-seq) from adult wild-type mice, postoperative day (POD) 14 mice and hADSC-Exos-treated postoperative day (POD) 14 mice. hADSC-Exos influences epithelial cells and fibroblasts, leading to scar-free wound healing. Among epithelial cell subtypes, Lef1high proliferating keratinocytes (prolif KC) are particularly remodeled by hADSC-Exos. Prolif KC exhibit epithelial-mesenchymal plasticity (EMP). The cell-cell communication between keratinocytes and fibroblasts in anti-scar healing is modulated by TGF-β1, which promote EMP transition cascade. hADSC-Exos may inhibit wound fibrosis through the 14-3-3Zeta-YES-associated protein (YAP)-hippo signaling pathway. This study enhances our understanding of epithelial cell diversity and interactions in wound healing, highlighting hADSC-Exos-induced prolif KC as potential reprogramming targets. These epithelial cells present promising therapeutic targets for improving wound healing strategies.
2025-06-03 | GSE298086 | GEO
Project description:The goal of our present work was to understand the influence parvovirus B19 infection may have on the thyroid hormone signaling pathway, as well as the nuclear receptors (NR) pathway overall. We demonstrated that B19 infection of CD36+ erythroid progenitor cells leads to downregulation of the thyroid hormone receptor α isoform. In addition to that we have shown that B19 infection modulates the expression of other members of the NR superfamily such as estrogen and retinoid receptors.
2012-11-04 | GSE42005 | GEO
Project description:Adipocyte dysfunctuon exacerbates obesity, yet the onset of adipocyte dysfunction is still unclear. Here, we employed RNA-seq and ATAC-seq on visceral adipose tissue from individuals with obesity or normal weight.Our research identified differentially expressed genes (DEGs) of VAT from individuals with normal wight or obesity enriched in pathways related to adipocyte metabolic function, thyroid hormone receptor binding sites were discovered in the accessible chromatin regions of these DEGs, including STAT5B. Motif enrichment, CHIP assay and in vitro cell experiments confirmed the decreased activation of STAT5B by triiodothyronine (T3) through binding with thyroid hormone receptor alpha (THRa) in obesity. In addition, RNA interference revealed STAT5B as a key transcription factor in maintaining the metabolic function of VAT. In conclusion, the impaired metabolic function of VAT is associated with altered chromatin accessibility to thyroid hormone (TH) in obesity. STAT5B is a key transcription factor at the core of the disrupted thyroid-adipose signaling and might be a promising target to improve obesity.
2025-05-19 | GSE286534 | GEO
Project description:Adipocyte dysfunctuon exacerbates obesity, yet the onset of adipocyte dysfunction is still unclear. Here, we employed RNA-seq and ATAC-seq on visceral adipose tissue from individuals with obesity or normal weight.Our research identified differentially expressed genes (DEGs) of VAT from individuals with normal wight or obesity enriched in pathways related to adipocyte metabolic function, thyroid hormone receptor binding sites were discovered in the accessible chromatin regions of these DEGs, including STAT5B. Motif enrichment, CHIP assay and in vitro cell experiments confirmed the decreased activation of STAT5B by triiodothyronine (T3) through binding with thyroid hormone receptor alpha (THRa) in obesity. In addition, RNA interference revealed STAT5B as a key transcription factor in maintaining the metabolic function of VAT. In conclusion, the impaired metabolic function of VAT is associated with altered chromatin accessibility to thyroid hormone (TH) in obesity. STAT5B is a key transcription factor at the core of the disrupted thyroid-adipose signaling and might be a promising target to improve obesity.
2025-05-19 | GSE286532 | GEO
Project description:Thyroid hormone is crucial for normal brain development. Thyroid hormone transporters control thyroid hormone homeostatis in brain. Mutations in the thyroid hormone transporter MCT8 result in a complex endocrine and neurological phenotype. We investigated the mechanisms of disease by analyzing gene expression profiles in fibroblasts from patients with mutations in MCT8. Performing comparative transcriptome analysis, we linked the genes differentially expressed in patient fibroblasts to the human brain transcriptome.
2010-08-23 | GSE20538 | GEO