91d000fe-ebb7-4557-b68d-9ce79cf228ba - samples
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PROVIDER: EGAD00001006801 | EGA |
REPOSITORIES: EGA
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Project description:Primary dermal fibroblasts from patients with dSSc and healthy controls were treated with TGF beta for up to 24h and the genome-wide patterns of gene expression measured on DNA microarrays. 894 genes were identified as TGF beta-responsive in 4 independent cultures of dermal fibroblasts (2 healthy control and 2 dSSc patients). The 894 genes in the TGF beta-responsive signature are associated with induction of growth factor signaling, collagen synthesis and extracellular matrix deposition.
2009-09-15 | GSE12493 | GEO
Project description:Transforming growth factor-Ã?1 (TGF-Ã?1, Uniprot: P01137) is a heparin-binding protein that has been implicated in a number of physiological processes, including the initiation of chondrogenesis by human mesenchymal stem cells (hMSCs). Here, we identify the molecular features in the protein and in heparin required for binding and their effects on the potentiation of TGF-Ã?1â??s activity on hMSCs. Using a proteomics â??Protect and Labelâ?? approach, lysines K291, K304, K309, K315, K338, K373, K375 and K388 were identified as being directly involved in binding heparin. Competition assays in an optical biosensor demonstrated that TGF-Ã?1 does require N- and 6-O-sulfate groups for binding but that 2-O-sulfate groups are unlikely to underpin the interaction. Heparin-derived oligosaccharides as short as degree of polymerization (dp) 4 have a weak ability to compete for TGF-Ã?1 binding to heparin, which increases with the length of the oligosaccharide to reach a maximum between dp18 and dp24. In cell-based assays, heparin, 2-O-, 6-O- and N-desulfated re-N-acetylated heparin and oligosaccharides 14â??24 saccharides (dp14â??24) in length all increased the phosphorylation of SMAD2 after 6 h of stimulation with TGF-Ã?1. The results provide the structural basis for a model of heparin/heparan sulfate binding to TGF-Ã?1 and demonstrate that the features in the polysaccharide required for binding are not identical to those required for sustaining the signaling by TGF-Ã?1 in hMSCs.
2016-07-19 | MSV000079921 | MassIVE
Project description:To determine if aberrant activation of endothelin-1 (Et1) could lead to the dysregulation of many downstream genes, we exposed fibroblasts to exogenous ET1 peptide and assayed for transcriptional changes by microarray. Mouse dermal fibroblasts were treated with exogenous Et1 peptide for 24 hours. ET1 treatment resulted in significant expression changes - primarily downregulation - of a number of genes. In particular, Tgf-beta-2 and Tgf-beta-3 were among the downregulated genes, which in turn alter the expression status of their many target genes. These data suggest that the stable silencing of Et1 is important for the phenotypic stability of dermal fibroblasts, and perhaps many other cell types as well.<br><br>Three separate biological replicates were derived for both control and treated samples. The primary dermal fibroblasts were derived by explant procedure from the skin of mouse pups aged 0-3 days. By passage 5, cells were split to two separate cultures-- one with 100nM synthetic Et1 peptide added to the medium (treated) and the other with nothing added (control). Cells were exposed to Et1 for 24 hrs, then treated and control populations were harvested for total RNA.
2007-06-29 | E-GEOD-4695 | biostudies-arrayexpress
Project description:Driving HUVECs toward mesenchymal fate Comparison of untreated HUVECs, HUVECs treated with TGF-B, HUVECS treated with TGF-B and oxidative stress, and comparator human dermal fibroblasts
2016-04-05 | E-GEOD-56309 | biostudies-arrayexpress
Project description:Recent studies in non-human model systems have shown therapeutic potential of modified mRNA (modRNA) treatments for lysosomal storage diseases. Here, we assessed the efficacy of a modRNA treatment to restore the expression of the α-galactosidase (GLA) gene in a human cardiac model generated from induced-pluripotent stem cell-derived from two patients with Fabry disease. In line with the clinical phenotype, cardiomyocytes from Fabry patient’s induced pluripotent stem cells show accumulation of the glycosphinolipid Globotriaosylceramide (GB3), which is an α-galactosidase substrate. Further, the patient-specific cardiomyocytes have significant upregulation of lysosomal associated proteins. Upon modRNA treatment, a subset of lysosomal proteins were partially restored to wildtype levels, implying the rescue of the molecular phenotype associated with the Fabry genotype. Importantly, a significant reduction of GB3 levels was observed in GLA modRNA treated cardiomyocytes demonstrating that α-galactosidase enzymatic activity was restored. Together, our results validate the utility of patient IPSC-derived cardiomyocytes as a model to study disease processes in Fabry disease and the therapeutic potential of GLA modRNA treatment to reduce GB3 accumulation in the heart.
2023-07-20 | PXD038361 | Pride
Project description:Filamentous algae (FA) have potential advantages over microalgae for wastewater treatment. However, their implementation at large-scale is hindered by an inability to predict performance. This study compared the cellular responses (photosynthesis and respiration) and composition (pigments and photosystem proteins) of FA Oedogonium acclimatised to average summer and winter conditions (Melbourne, Australia). After 7 days of acclimation the Chl a content of summer acclimated (SA) algae was about half that of the winter acclimated (WA) algae, which can be related to a strategy to reduce photodamage under high light intensities. No statistically significant changes were observed in any identified proteins associated with photosystem PSII and the reaction centre of PSI. Transmission electron microscopy images revealed more prominent lipid bodies within the SA filaments than in WA filaments, but no discernible difference in the abundance of starch granules. Photosynthetic irradiance curves were compared for the SA and WA algae. Consistent with the differences in chlorophyll, the specific gross photosynthetic rate (µP, gross) was generally higher for the WA algae. The relative difference increased from around 2-fold at 15°C to 3-fold at 25°C, and then decreased to less than 1.5-fold at 30 °C and 35 °C. At all the tested temperatures, saturation irradiance levels were in the range of 75 – 500 µmol/m2·s. Photoinhibition was observed at 30 °C (above ~300 µmol/m2·s) and was more severe at 35 °C (above ~500 µmol/m2·s), with WA algae showing greater inhibition. In contrast, the respiration response was similar for the SA and WA algae. The study emphasises the significance of accounting for seasonal variations and their effects on biomass productivity and utilisation. The data obtained will enable the incorporation of acclimation and its effect on biochemistry and photosynthetic response into predictive models of FA performance in outdoor cultures.
2026-01-12 | PXD040798 | Pride
Project description:Control human dermal fibroblasts from patient forearm
| EGAD00010001879 | EGA
Project description:Primary human dermal fibroblasts treated with TGF-b and/or MA-5
| PRJNA1347225 | ENA
Project description:Shprintzen-Goldberg syndrome (SGS) is a multisystemic connective tissue disorder, with considerable clinical overlap with Marfan and Loeys-Dietz syndromes. These syndromes have commonly been associated with enhanced TGF-β signaling. In SGS patients, heterozygous point mutations have been mapped to the transcriptional corepressor SKI, which is a negative regulator of TGF-β signaling that is rapidly degraded upon ligand stimulation. The molecular consequences of these mutations, however, are not understood. Here we use a combination of structural biology, genome editing and biochemistry to show that SGS mutations in SKI abolish its binding to phosphorylated SMAD2 and SMAD3. This results in stabilization of SKI and consequently attenuation of TGF-β responses, in both knockin cells expressing an SGS mutation, and in fibroblasts from SGS patients. Thus, we reveal that SGS is associated with an attenuation of TGF-β-induced transcriptional responses, and not enhancement, which has important implications for other Marfan-related syndromes.
| EGAS00001004908 | EGA