Transcriptome changes during Endothelial to Mesenchymal Transition (EndMT) using a TGF-b2 and IL-1b in vitro model of EndMT in HUVEC and HPAEC
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PROVIDER: PRJNA485688 | ENA |
REPOSITORIES: ENA
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Project description:Endothelial-to-mesenchymal transition (EndMT) is a dynamic transformation process that has a functional impact upon pathological vascular remodelling. However, the molecular mechanisms that govern EndMT remain largely unknown. We modelled this process in vitro by exposing human primary endothelial cells to a combination of transforming growth factor-β2 (TGF- β2) and interleukin-1β (IL-1β). RNAseq was carried out to analyse the change of gene expression during the transition and define the transcriptional architecture of EndMT.
2020-12-31 | GSE118446 | GEO
Project description:To investigate the transcriptome level changes in human bone marrow-derived mesenchymal stem cells following treatment with TGF-b2, we used RNA-sequencing to compare gene expression between cells from the same donors cultured in standard media or media containing 1 ng/ml TGF-b2.
2023-01-30 | GSE220294 | GEO
Project description:To investigate the transcriptome level changes in gene expression in equine mesenchymal stem cells following treatment with TGF-b2, we used RNA-sequencing to compare gene expression between mesenchymal stem cells from the same donor horses cultured in standard media and media containing TGF-b2.
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Project description:Growth Factor Independence-1B (Gfi-1B) is a transcriptional repressor essential for erythropoiesis and megakaryopoiesis. Targeted gene disruption of Gfi-1B in mice leads to embryonic lethality due to failure to produce definitive erythrocytes, hindering the study of Gfi-1B function in adult hematopoiesis. We here show that, in humans, Gfi-1B controls the development of erythrocytes and megakaryocytes by regulating the proliferation and differentiation of bipotent erythro-megakaryocytic progenitors (MEP). We further identify in this cell population the type III transforming growth factor-? receptor gene, TGFBR3, as a direct target of Gfi-1B. Knock down of Gfi-1B results in altered TGF? signaling as shown by the increase in Smad2 phosphorylation and its inability to associate to the Transcription Intermediary Factor 1? (TIF1?). Because Smad2/TIF1? complex is known to specifically regulate erythroid differentiation, we propose that, by repressing the transforming growth factor-? receptor III (T?R?II) expression, Gfi-1B favors the Smad2/TIF1? interaction downstream of TGF? signaling, allowing immature progenitors to differentiate toward the erythroid lineage.
2010-04-19 | E-MEXP-2560 | biostudies-arrayexpress
Project description:IL-1B is an important cytokine that is often found to be up-regulated during osteoarthritic and rheumatoid joint diseases. It is viewed as a catabolic factor, inducing enzymes that allow for the degradation of the cartilage extracellular matrix and also has essential roles as an autocrine and paracrine factor in fibronectin fragment-mediated degradation. It can also reduce the synthesis of the major cartilage components, type II collagen and aggrecan. On the other hand, IL-1B also has the ability to induce the growth and morphogenic factor BMP-2. During joint diseases, IL-1B is synthesized by both synovial cells and chondrocytes. Addition of IL-1 biological antagonists such as IL-1 receptor antagonists can suppress cartilage degradation in vitro. Thus, the production of IL-1B could act as the first step in mediating a cascade of other mediators in cartilage which could be relevant to the fate of the cartilage. In order to obtain a global picture of the effect of IL-1B production on human adult articular chondrocytes, we analyzed changes in gene expression induced by IL-1B by microarray analysis. We found that IL-1B has a diverse effect on gene expression profile in chondrocytes. One of the predominant responses that we observed in adult human articular chondrocytes on exposure to IL-1B is a dramatic increase in a large set of chemokines and other genes related to the inflammatory cascade. Keywords: Gene response to IL-1B (10 ng/ml) Cartilage was obtained from adult human tissue donors with above the knee amputations due to chondrosarcoma or traumatic injury or from autopsy. Chondrocytes were isolated following established protocols, maintained in high density, and treated with IL-1B (10 ng/ml). Chondrocytes treated with buffer only served as the untreated control. The experiment was carried out in duplicate. Total RNA was extracted from these chondrocytes, labeled with fluorophores (Cy3 or Cy5) and analyzed for expression changes using the Human Operon/Qiagen v3.0 oligonucleotide array. The analysis was repeated with the fluorophore dyes exchanged between the untreated and experimental RNAs.
2008-05-14 | E-GEOD-11427 | biostudies-arrayexpress
Project description:IL-1B is an important cytokine that is often found to be up-regulated during osteoarthritic and rheumatoid joint diseases. It is viewed as a catabolic factor, inducing enzymes that allow for the degradation of the cartilage extracellular matrix and also has essential roles as an autocrine and paracrine factor in fibronectin fragment-mediated degradation. It can also reduce the synthesis of the major cartilage components, type II collagen and aggrecan. On the other hand, IL-1B also has the ability to induce the growth and morphogenic factor BMP-2. During joint diseases, IL-1B is synthesized by both synovial cells and chondrocytes. Addition of IL-1 biological antagonists such as IL-1 receptor antagonists can suppress cartilage degradation in vitro. Thus, the production of IL-1B could act as the first step in mediating a cascade of other mediators in cartilage which could be relevant to the fate of the cartilage. In order to obtain a global picture of the effect of IL-1B production on human adult articular chondrocytes, we analyzed changes in gene expression induced by IL-1B by microarray analysis. We found that IL-1B has a diverse effect on gene expression profile in chondrocytes. One of the predominant responses that we observed in adult human articular chondrocytes on exposure to IL-1B is a dramatic increase in a large set of chemokines and other genes related to the inflammatory cascade. Keywords: Gene response to IL-1B (10 ng/ml)
2008-05-14 | GSE11427 | GEO
Project description:Cytokines have been shown to play a key role in the destruction of beta cells. In the rat insulinoma cell line (INS-1ab) overexpressing pancreatic duodenum homeobox 1 (Pdx1) increases sensitivity to Interleukin 1b (IL-1b). To elucidate mechanisms of action underlying Pdx1 driven potentiation of beta-cell sensitivity to IL-1β, we performed a microarray analysis of INS-1ab cells with and without Pdx1 overexpression exposed to IL-1β between 2h and 24h. INS-1ab cells were cultured with or without 500 ng/ml doxycycline (+/- DOX). After 24 h, 40 ng/ml IL-1b was either added or not (+/- IL-1b). Cells were harvested either 2h, 4h, 6h, 12h or 24h after addition of IL-1b. Four biological replicates for each of the eight groups.
2012-09-20 | E-GEOD-40642 | biostudies-arrayexpress
Project description:To investigate the response of Th17 cells to IL-1B and Dexamethasone, and the ability of IL-B to alter the steroid-responsiveness of Th17 cells
2024-04-30 | GSE230417 | GEO
Project description:TGF-b2 drives catalase transcription to regulate tumor H2O2 levels, and Theileria gene expression in transformed macrophages
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Project description:This program aims at identifying the lung gene signature associated with inflammation and emphysema in IL-1b-Tg mouse COPD model to facilitate understanding of the disease mechanism and therapeutic compound testing The lung profiling data was analyzed by identifying genes that were up- and down-regulated at selected p value and fold change in the lungs of IL-1b-Tg mice treated with doxycycline (to induce IL-1b transgene) compared to the corresponding water-treated controls.
2013-03-22 | E-GEOD-38075 | biostudies-arrayexpress