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To examine the expression of Sulf1 and Sulf2, as well as other glycan-related genes, in human Idiopathic pulmonary fibrosis (IPF) lungs compared to normal lung samples

ABSTRACT: Microarray analysis to examine glycan-related gene expression in idiopathic pulmonary fibrosis Heparan sulfate 6-O-endosulfatases (Sulf1 and Sulf2) remove 6-O sulfate groups from heparan sulfate intra-chain sites on the cell surface and in the extracellular matrix, and modulate the functions of many growth factors and morphogens including FGF, Wnt and TGF-beta. Works from our laboratory have shown that TGF-beta 1 induces Sulf1 and Sulf2 expression in a cell-type specific manner in the lung, specifically Sulf1 in lung fibroblasts and Sulf2 in type II alveolar epithelial cells. Interestingly TGF-beta 1-induced Sulf1 and Sulf2 in turn modulate TGF-beta 1 function in culture.

ORGANISM(S): Homo sapiens

PROVIDER: GSE31934 | GEO | 2011/09/06

SECONDARY ACCESSION(S): PRJNA145033

REPOSITORIES: GEO

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To examine the expression of Sulf1 and Sulf2, as well as other glycan-related genes, in human Idiopathic pulmonary fibrosis (IPF) lungs compared to normal lung samples

Project description:Microarray analysis to examine glycan-related gene expression in idiopathic pulmonary fibrosis Heparan sulfate 6-O-endosulfatases (Sulf1 and Sulf2) remove 6-O sulfate groups from heparan sulfate intra-chain sites on the cell surface and in the extracellular matrix, and modulate the functions of many growth factors and morphogens including FGF, Wnt and TGF-beta. Works from our laboratory have shown that TGF-beta 1 induces Sulf1 and Sulf2 expression in a cell-type specific manner in the lung, specifically Sulf1 in lung fibroblasts and Sulf2 in type II alveolar epithelial cells. Interestingly TGF-beta 1-induced Sulf1 and Sulf2 in turn modulate TGF-beta 1 function in culture. The aim of this study is to examine the expression of Sulf1 and Sulf2 as well as other glycan-related genes (heparan biosynthetic enzymes, TGF-beta, FGF and Wnt signaling pathway components) in human idiopathic pulmonary fibrosis (IPF) lungs compared to normal lung samples. We will examine gene expression in triplicate samples from RNA of total lung homogenates from IPF and control (normal) lungs

2011-09-05 | E-GEOD-31934 | biostudies-arrayexpress

Identification of SULF2 as a novel transcriptional target of p53 by use of integrated genomic analyses.

Project description:Microarray analysis has been useful for identifying the targets of many transcription factors. However, gene expression changes in response to transcription factor perturbation reveal both direct transcriptional targets and secondary gene regulation. By integrating RNA interference, gene expression profiling, and chromatin immunoprecipitation technologies, we identified a set of 32 direct transcriptional targets of the tumor suppressor p53. Of these 32 genes, 11 are not currently associated with the core p53 pathway. From among these novel pathway members, we focused on understanding the connection between p53 and SULF2, which encodes an extracellular heparan sulfate 6-O-endosulfatase that modulates the binding of growth factors to their cognate receptors and that has been shown to function as a tumor suppressor. Genetic and pharmacologic perturbation of p53 directly influences SULF2 expression, and similar to silencing of TP53, RNA interference-mediated suppression of SULF2 results in an impaired senescence response of cells to genotoxic stress. Thus, our integrated genomic approach has led to the identification of a novel mediator of p53 network biology. Expression profiling experiments were performed to perturb the p53 status in cancer cell lines as a means of identifying novel members of the p53 pathway.

2010-06-20 | E-GEOD-15440 | biostudies-arrayexpress

Heparan sulfate modifications of betaglycan promote TIMP3-dependent ectodomain shedding to fine-tune TGF-β signaling.

Project description:Betaglycan/type III TGF-β receptor (TGFBR3) is an established co-receptor for the TGF-β superfamily with direct binding demonstrated for TGF-β 1-3 and inhibin A. Betaglycan can be membrane-bound or have its ectodomain cleaved/ shed to produce soluble-betaglycan that has been demonstrated to sequester ligands. Extracellular domain of betaglycan is modified with glycosaminoglycan chains at Ser residues S534 and S545, to which heparan sulfate and chondroitin sulfate chains are covalently attached. To delineate the contribution of the heparan and chondroitin sulfate modifications on betaglycan on its shedding and thereby on TGF-β signaling in ovarian cancer biology, we used mutants of betaglycan with alterations to the different glycosaminoglycan modifications. We made the unexpected discovery that the heparan sulfate modifications are essential for maximum ectodomain shedding of betaglycan, which is further essential for the ability of betaglycan to suppress TGF-β signaling and the tumor cells responses to exogenous TGF-β ligand. Using unbiased transcriptomics, we identified TIMP3 as a key regulator of betaglycan shedding and thereby TGF-β signaling. Taken together, these studies are the first to demonstrate a critical link between the well-known modifications on betaglycan and TGF-β signaling responses.

2024-02-21 | GSE237403 | GEO

Identification of SULF2 as a novel transcriptional target of p53 by use of integrated genomic analyses.

2009-04-01 | GSE15440 | GEO

Examine differential expression of sulf-1 and sulf-2, enzymes involved in heparan sulfate biosynthesis

2011-04-29 | GSE28931 | GEO

Investigating the role of GLI1 in SULF2-potentiated liver tumorigenesis

Project description:The expression of the extracellular sulfatase, SULF2, has been strongly associated with increased hepatocellular carcinoma (HCC) tumor growth and poorer patient survival. However, to date, the molecular mechanisms underlying this phenomenon remain in part unclear. To address this issue, we developed a transgenic mouse overexpressing Sulf2 in hepatocytes under the control of the transthyretin promoter. In this mouse model Sulf2 overexpression potentiated DEN-induced HCC. Further analysis demonstrated a central role for the zinc finger transcription factor Gli1 as a mediator of Sulf2 during HCC development. The cross of the Sulf2 transgenic with Gli1 knockout mice showed that the inactivation of this transcription factor impaired Sulf2-induced HCC. Transcriptomic analysis revealed a Stat3 gene signatures associated with Sulf2 overexpression. Interestingly, Gli1 knockout abrogates Sulf2-induction of several Stat3 target genes including Socs2/3, Pim1 and Flt4. Human orthologues were similarly regulated by SULF2 and dependent on intact GLI1 and STAT3 function in human HCC cells. SULF2 overexpression not only resulted in GLI1 and STAT3 interaction, but also promoted enrichment of GLI1 and STAT3 at consensus sites at the target gene promoters. Interestingly, GLI1 was found to be enriched at select STAT3 consensus sites with SULF2 overexpression and vice versa. siRNA-mediated knockdown of STAT3 or GLI1 reduced promoter binding of GLI1 and STAT3 respectively. Finally, chromatin capture PCR confirmed long-range co-regulation of SOCS2 and FLT3 through changes in promoter conformation. Thus, these findings define a novel mechanism by which SULF2 drives HCC and highlights the role of GLI1-STAT3 transcriptional complex as an effector of this sulfatase.

2019-10-25 | GSE139374 | GEO

Examine differential expression of sulf-1 and sulf-2, enzymes involved in heparan sulfate biosynthesis

Project description:Our specific aim is to examine differential expression of sulf-1 and sulf-2, enzymes involved in heparan sulfate biosynthesis, as well as Wnt ligands and Wnt signaling mediators during corneal wound healing using a mouse corneal scratch model. The specific structural features of heparan sulfate underlie its role in modulating cellular responses to growth factors such as the Wnts. Heparan sulfate 6-O-endosulfatases (sulf-1 and sulf-2) remove 6-O sulfate group from trisulfated disaccharides present on heparan sulfate chains. Our preliminary results suggest that sulf-1 is upregulated at the protein level in the epithelial cells of wounded mouse corneas, as compared to the undamaged contralateral eye. Modulation of heparan sulfate proteoglycan expression and/or structural modifications of its chains might be an important aspect of the regulation of epithelial cell migration and proliferation during wound healing. RNA preparations from four different conditions, were sent to Microarray Core (E). Gene expression was examined in triplicates at 2 time points (8 and 24 hrs post-wounding: 6 arrays), using the contralateral eye as a control at one time point as a control (3 arrays). To account for a systemic response (i.e. bilateral inflammation) to the corneal wounding, corneas of non-wounded mice (3 arrays) were used. The RNA was amplified, labeled, and hybridized to the GLYCOv3 microarrays.

2011-04-29 | E-GEOD-28931 | biostudies-arrayexpress

Transcriptome profile in SULF2 knockdown pancreatic tumor cells

Project description:We constructed the SULF2 knockdown cell lines and its controls in CFPAC-1 cells using CRISPR-cas9 system, followed by transcriptome sequencing.

2022-03-02 | GSE197531 | GEO

Recapitulation of pharmacogenomic data reveals that invalidation of SULF2 enhance sorafenib susceptibility in liver cancer

Project description:Gene mutations play critical roles during cancer development and progression, and therefore represent targets for precision medicine. Here we recapitulated the pharmacogenomic data to delineate novel candidates for actionable mutations and therapeutic target drugs. As a proof-of-concept, we demonstrated that the loss-of-function of SULF2 by mutation (N491K) or inhibition enhanced sorafenib sensitivity in liver cancer cells and in vivo mouse models. This effect was mediated by deregulation of EGFR signaling and downstream expression of LCN2. We also report that the liver cancer patients non-responding to sorafenib treatment exhibit higher expression of SULF2 and LCN2. In conclusion, we suggest that SULF2 plays a key role in sorafenib susceptibility and resistance in liver cancer via deregulation of LCN2. Diagnostic or therapeutic targeting of SULF2 (e.g., OKN-007) and/or LCN2 can be a novel precision strategy for sorafenib treatment in cancer patients.

2018-05-15 | GSE88744 | GEO

Expression data from adult mice pulmonary endothelial cells

Project description:Sepsis patients are at increased risk for hospital-acquired pulmonary infections, potentially due to post-septic immunosuppression known as the compensatory anti-inflammatory response syndrome (CARS). CARS has been attributed to leukocyte dysfunction, with an unclear role for endothelial cells. The pulmonary circulation is lined by an endothelial glycocalyx, a heparan sulfate-rich layer essential to pulmonary homeostasis. Heparan sulfate degradation occurs early in sepsis, leading to lung injury. Endothelial synthesis of new heparan sulfates subsequently allows for glycocalyx reconstitution and endothelial recovery. We hypothesized that remodeling of the reconstituted endothelial glycocalyx, mediated by alterations in the endothelial machinery responsible for heparan sulfate synthesis, contributes to CARS. Our experimental animal model of CARS recapitulated post-septic immunosuppression, coincidentally with structural remodeling of endothelial glycocalyx heparan sulfate. We used microarray to identify which heparan sulfate modifying enzyme is responsible for the remodeling of post-septic reconstituted glycocalyx, characterized with enrichment of heparan sulfate disaccharides sulfated at the 6-O position of glucosamine.

2019-04-14 | GSE129775 | GEO

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