ArticleThe Journal of biological chemistry2008
Transforming growth factor-beta1 induces heparan sulfate 6-O-endosulfatase 1 expression in vitro and in vivo.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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46 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
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- Myeloid deficiency of heparan sulfate 6-O-endosulfatases impairs bone marrow hematopoiesis.Matrix biology : journal of the International Society for Matrix Biology · 2024Article
- SULF1 expression is increased and promotes fibrosis through the TGF-β1/SMAD pathway in idiopathic pulmonary fibrosis.Journal of translational medicine · 2024Article
- [Identification of SULF1 as a Shared Gene in Idiopathic Pulmonary Fibrosis and Lung Adenocarcinoma].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2023Article
- Extracellular sulfatase-2 is overexpressed in rheumatoid arthritis and mediates the TNF-α-induced inflammatory activation of synovial fibroblasts.Cellular & molecular immunology · 2022Article
- PTPα promotes fibroproliferative responses after acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Context Dependent Sulf1/Sulf2 Functional Divergence in Endothelial Cell Activity.International journal of molecular sciences · 2022Article
- LncRNAInternational journal of molecular sciences · 2021Article
- Heparan Sulfate Proteoglycans Biosynthesis and Post Synthesis Mechanisms Combine Few Enzymes and Few Core Proteins to Generate Extensive Structural and Functional Diversity.Molecules (Basel, Switzerland) · 2020Review
- Glutamyl-Prolyl-tRNA Synthetase Regulates Proline-Rich Pro-Fibrotic Protein Synthesis During Cardiac Fibrosis.Circulation research · 2020Article
- Changes in heparan sulfate sulfotransferases and cell-surface heparan sulfate during SKM-1 cells granulocytic differentiation and A549 cells epithelial-mesenchymal transition.Glycoconjugate journal · 2020Article
- The histone demethylase JMJD2B regulates endothelial-to-mesenchymal transition.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Identification of transcriptomic markers for developing idiopathic pulmonary fibrosis: an integrative analysis of gene expression profiles.International journal of clinical and experimental pathology · 2020Article
- 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
- HDAC8 inhibition ameliorates pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Fasudil and DETA NONOate, Loaded in a Peptide-Modified Liposomal Carrier, Slow PAH Progression upon Pulmonary Delivery.Molecular pharmaceutics · 2018Article
- Epithelial Deletion of Sulf2 Exacerbates Bleomycin-Induced Lung Injury, Inflammation, and Mortality.American journal of respiratory cell and molecular biology · 2017Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Transforming growth factor (TGF)-beta1 plays an important role in the development of pulmonary fibrosis. In this study we examined the relationship between TGF-beta1 stimulation and the expression of heparan sulfate (HS) 6-O-endosulfatase 1 (Sulf1) in cultured normal human lung fibroblasts (NHLFs) and in murine lungs in vivo. By removing 6-O-sulfates from specific HS intrachain sites on the cell surface, Sulf1 has been shown to modulate the activities of many HS binding growth factors and morphogens including fibroblast growth factor (FGF)-2. Real time reverse transcription-PCR analysis revealed that TGF-beta1 increased Sulf1 expression in NHLFs in a dose- and time-dependent manner which was accompanied by a decrease in 6-O-sulfated disaccharides as revealed by high performance liquid chromatography analysis. Decreased ERK activation after FGF-2 stimulation was observed in TGF-beta1-treated NHLFs compared with control cells without changes in HS-dependent FGF-2 binding or FGF-2.FR1c complex formation. To study the function of Sulf1, negative control or Sulf1-specific small interference RNA (siRNA)-transfected NHLFs were stimulated with TGF-beta1. Enhanced Smad2/3 phosphorylation and elevated total Smad2 protein level were observed in Sulf1 siRNA-transfected cells and were accompanied by enhanced expression of alpha-smooth muscle actin and fibronectin. In addition, Sulf1 siRNA transfection enhanced the anti-proliferative effect of TGF-beta1. Finally Sulf1 expression was up-regulated in the lungs of mice treated with adenovirus encoding active TGF-beta1. Taken together, our data indicate that Sulf1 is a TGF-beta1-responsive gene both in vitro and in vivo and may function as a negative regulator of TGF-beta1-induced fibrogenesis.
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