Similar Datasets
Project description:Gene expression profiles associated with ITGBL1 overexpression
| PRJNA699005 | ENA
Project description:Elevated intraocular pressure (IOP) is the major risk factor for glaucoma. The molecular mechanism of elevated IOP is unclear, which impedes glaucoma therapy. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible Poly-ADP-ribose Polymerase (TIPARP), a member of the PARP family, catalyses mono-ADP-ribosylation. Here we showed that TIPARP was widely expressed in the cornea, trabecular meshwork, iris, retina, optic nerve, sclera, and choroid of human eyes. The expression of TIPARP was significantly upregulated in the blood and trabecular meshwork of patients with primary open angle glaucoma compared with that of healthy controls. Transcriptome analysis revealed that the expression of genes related to extracellular matrix deposition and cell adhesion was decreased in TIPARP-upregulated human trabecular meshwork (HTM) cells. Moreover, western blot analysis showed that collagen types I and IV, fibronectin, and α-SMA were increased in TIPARP downregulated or TIPARP-inhibited HTM cells. In addition, cross-linked actin networks were produced, and vinculin was upregulated in these cells. Subconjunctival injection of the TIPARP inhibitor RBN-2397 increased the IOP in Sprague–Dawley rats. Therefore, we identified TIPARP as a regulator of IOP through modulation of extracellular matrix and cell cytoskeleton proteins in HTM cells. These results indicate that TIPARP is a potential therapeutic target for ocular hypertension and glaucoma.
2022-12-28 | GSE218153 | GEO
Project description:SPRR1A-overexpression did not alter the gene expression profiles associated with aggressive progression of PDAC
2022-03-27 | GSE186935 | GEO
Project description:Histone deacetylases (HDAC) are epigenetic regulators of trascription. Preclinical studies have determined that HDAC inhibition can prevent kidney interstitial fibrosis in acute kidney injury. The purpose of this study was to determine if overexpression of HDAC1 in kidney fibroblasts significantly affects the fibroblast transcriptome. Transforming growth factor beta-1 (TGFB1) causes fibroblasts to differentiate into myofibroblasts leading to extracelluar matrix secretion. A subset of our cells were treated with TGFB1 for 24 hours to determine if this in combination with HDAC1 overexpression significantly alters the transcriptomes.
2025-11-24 | GSE310601 | GEO
Project description:TRIM24 (Tripartite Motif-Containing 24) is a key transcriptional co-regulator involved in various cellular processes, including chromatin remodeling and gene expression. However, its role in cardiomyocytes remains largely unexplored. In this study, we investigated the global proteomic changes associated with TRIM24 overexpression in neonatal rat ventricular cardiomyocytes (NRVCMs) to better understand its function in cardiac biology. NRVCMs were transduced by an Adenovirus overexpressing TRIM24. Protein isolated from the NRVCMs transduced by an Adenovirus overexpressing LacZ was used as control.
2025-07-14 | PXD064832 | Pride
Project description:Chondrocytes are the only cell type in cartilage and play a pivotal role in tissue homeostasis and cartilage remodeling in Osteoarthritis (OA). OA-dependent metabolic changes affecting extracelluar matrix composition as well as variations in the response to cytokines and growth factors have been investigated in human chondrocytes. However, the molecular mechanisms causing age-dependent variation of the chondrocyte phenotype are poorly characterized. The proinflammatory mediator nitric oxide (NO) is produced when chondrocytes are exposed to cytokines such as IL-1. NO affects the energy metabolism of cells through interfering with mitochondrial respiration and glycolysis and has been implicated in extracellular matrix synthesis and degradation and chondrocyte death. NO may contribute to the aging process by compromising the energy balance in chondrocytes through the generation of an oxidizing environment and this may in turn affect matrix gene expression. In human chondrocytes NO effects on the expression of extacelluar matrix genes or genes related to matrix structure have not been addressed comprehensively.
2011-02-17 | GSE27358 | GEO
Project description:In vitro disease modeling of an erly B cell factor 2 (EBF2) nonsense variant (EBF2 8:26033143 C>A, c.493G>T, p.E165X) demonstrates that the EBF2 variant impairs adipogenesis causing excess accumulation of extracelluar matrix protein and inflammatory myeloid cells.
2025-02-17 | GSE288824 | GEO
Project description:Chondrocytes are the only cell type in cartilage and play a pivotal role in tissue homeostasis and cartilage remodeling in Osteoarthritis (OA). OA-dependent metabolic changes affecting extracelluar matrix composition as well as variations in the response to cytokines and growth factors have been investigated in human chondrocytes. However, the molecular mechanisms causing age-dependent variation of the chondrocyte phenotype are poorly characterized. The proinflammatory mediator nitric oxide (NO) is produced when chondrocytes are exposed to cytokines such as IL-1. NO affects the energy metabolism of cells through interfering with mitochondrial respiration and glycolysis and has been implicated in extracellular matrix synthesis and degradation and chondrocyte death. NO may contribute to the aging process by compromising the energy balance in chondrocytes through the generation of an oxidizing environment and this may in turn affect matrix gene expression. In human chondrocytes NO effects on the expression of extacelluar matrix genes or genes related to matrix structure have not been addressed comprehensively. In this study cultured chondrocytes from a single donor was either be left unstimulated (control) or stimulated with IL-1, L-NMMA or IL-1 L-NMMA for a period of 8 days in order to achieve sufficiently high levels of intracellular NO and stable expression of a subset of genes. Samples were hybridized and analyzed using the GLYCOv2 array. L-NMMA (NG-monomethyl-L-arginine) is a competitive inhibitor NO synthesis.
2011-02-17 | E-GEOD-27358 | biostudies-arrayexpress
Project description:We previously reported that TCDD-inducible poly-ADP-ribose polymerase (TIPARP), an aryl hydrocarbon receptor (AHR) target gene and mono-ADP-ribosyltransferase, acts as part of a negative feedback loop to repress AHR signalling, a process that prevented by a single H532A mutation that destroys TIPARP catalytic activity. Moreover, whole body or hepatocyte specific-deletion of, increases the sensitivity of mice to dioxin-induced toxicities. Based on these findings, we hypothesized that the loss of TIPARP catalytic activity would increase sensitivity to TCDD-induced toxicity in vivo. To test the hypothesis, we created a catalytically deficient mouse line (TiparpH532A) by introducing a single H532A mutation in Tiparp. Treatment of mouse embryonic fibroblasts (MEFs) or hepatocytes isolated from TiparpH532A mice confirmed the increased TCDD-induced expression of the AHR target genes, Cyp1a1, Cyp1b1 and Tiparp. We also confirmed TCDD-dependent increases in Tiparp protein levels, as well as increased protein stabilization of TiparpH532A compared Tiparp+/+ protein. TiparpH532A mice given a single injection of 10 ug/kg dioxin, a non-lethal dose in Tiparp+/+ mice, did not survive beyond day 10. All Tiparp+/+ mice survived the 30-day treatment. Dioxin treated TiparpH532A mice displayed increased expression of Ahr target genes, increased steatohepatitis and hepatotoxicity as indicated by increased alanine aminotransferase activity compared with wildtypes. Taken together, these data further support TIPARP as a key negative regulator of AHR activity and its specific loss of its catalytic activity is sufficient to increase the sensitivity to dioxin-induced hepatosteatosis and lethality. TIPARP has recently emerged as a potential anti-cancer therapeutic; however, AHR signalling and toxicity will need to be carefully considered in determining the consequences of TIPARP inhibition.
2021-09-08 | GSE167205 | GEO