ArticleGlycobiology2013
Overexpression of Sulf2 in idiopathic pulmonary fibrosis.
Article in Glycobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- Analysis of Allele-Specific Expression Highlights Novel Participants of Empagliflozin-Driven Effects on T2DM-Associated Regulatory Pathways.International journal of molecular sciences · 2026Article
- Heparan-6-O-endosulfatase 2, a cancer-related proteoglycan enzyme, is effectively inhibited by a specific sea cucumber fucosylated glycosaminoglycan.Glycobiology · 2025Article
- Myeloid deficiency of heparan sulfate 6-O-endosulfatases impairs bone marrow hematopoiesis.Matrix biology : journal of the International Society for Matrix Biology · 2024Article
- Sulfatase-2 from Cancer Associated Fibroblasts: An Environmental Target for Hepatocellular Carcinoma?Liver cancer · 2022Article
- A Markov random field model for network-based differential expression analysis of single-cell RNA-seq data.BMC bioinformatics · 2021Article
- Article
- New insights into the pathogenesis of Peyronie's disease: A narrative review.Chronic diseases and translational medicine · 2020Review
- HS and Inflammation: A Potential Playground for the Sulfs?Frontiers in immunology · 2020Review
- Syndecan-4 Inhibits the Development of Pulmonary Fibrosis by Attenuating TGF-β Signaling.International journal of molecular sciences · 2019Article
- MicroRNA-422a functions as a tumor suppressor in non-small cell lung cancer through SULF2-mediated TGF-β/SMAD signaling pathway.Cell cycle (Georgetown, Tex.) · 2019Article
- Mass spectrometry analysis of the human endosulfatase Hsulf-2.Biochemistry and biophysics reports · 2019Article
- OKN-007 Increases temozolomide (TMZ) Sensitivity and Suppresses TMZ-Resistant Glioblastoma (GBM) Tumor Growth.Translational oncology · 2019Article
- Epithelial Deletion of Sulf2 Exacerbates Bleomycin-Induced Lung Injury, Inflammation, and Mortality.American journal of respiratory cell and molecular biology · 2017Article
- The "in and out" of glucosamine 6-O-sulfation: the 6th sense of heparan sulfate.Glycoconjugate journal · 2017Review
- Detecting the Molecular System Signatures of Idiopathic Pulmonary Fibrosis through Integrated Genomic Analysis.Scientific reports · 2017Article
- Overexpression of heparanase attenuated TGF-β-stimulated signaling in tumor cells.FEBS open bio · 2017Article
- Impact of Sulfatase-2 on cancer progression and prognosis in patients with renal cell carcinoma.Cancer science · 2016Article
- Heparan Sulfate in the Developing, Healthy, and Injured Lung.American journal of respiratory cell and molecular biology · 2016Review
- Design and synthesis of biphenyl and biphenyl ether inhibitors of sulfatases.Chemical science · 2016Article
- Differences between Mice and Humans in Regulation and the Molecular Network of Collagen, Type III, Alpha-1 at the Gene Expression Level: Obstacles that Translational Research Must Overcome.International journal of molecular sciences · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Previously, we have shown that heparan sulfate (HS) 6-O-endosulfatase 1 (Sulf1) is a transforming growth factor-β1 (TGF-β1)-responsive gene in normal human lung fibroblasts and functions as a negative feedback regulator of TGF-β1 and that TGF-β1 induces the expression of Sulf1 as well as that of the closely related Sulf2 in a murine model of pulmonary fibrosis. In this study, we focused on the role of Sulf2 in modulating TGF-β1 function and the development of pulmonary fibrosis. We found that Sulf2 mRNA was overexpressed in lung samples from human patients with idiopathic pulmonary fibrosis (IPF), and Sulf2 protein was specifically localized to the hyperplastic type II alveolar epithelial cells (AECs). In vitro, TGF-β1 induced the expression of Sulf2 with accompanied HS 6-O-desulfation in A549 cells, adenocarcinoma cells derived from the type II alveolar epithelium. Using small interference RNA to block Sulf2 expression, we observed a biphasic TGF-β1 response with early enhanced Smad activation, but eventually reduced TGF-β1 target gene expression in Sulf2 knockdown A549 cells compared with the control cells. To study the role of Sulf2 in normal type II AECs, we isolated primary type II cells from wild-type and Sulf2 knockout mice. We observed enhanced Smad activation as well as enhanced TGF-β1 target gene expression in Sulf2 knockout type II AECs compared with wild-type type II AECs. In conclusion, Sulf2 is overexpressed in IPF and may play a role in regulating TGF-β1 signaling in type II AECs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.