ArticlePloS one2012
Syndecan-2 is a novel target of insulin-like growth factor binding protein-3 and is over-expressed in fibrosis.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- The Relationship between Time, Race, and Estrogen Receptor Alpha in Estradiol-Induced Dermal Fibrosis.Biomedicines · 2024Article
- Integrated Bioinformatic Analysis of Differentially Expressed Genes Associated with Wound Healing.Cell journal · 2023Article
- The Molecular Mechanisms of Systemic Sclerosis-Associated Lung Fibrosis.International journal of molecular sciences · 2023Review
- Syndecan-2 selectively regulates VEGF-induced vascular permeability.Nature cardiovascular research · 2022Article
- How Do We Know What We Are Missing? Loss of Signaling through CD148 Drives Fibroblast Activation in Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2021Article
- Syndecan receptors: pericellular regulators in development and inflammatory disease.Open biology · 2021Review
- Pulmonary involvement in systemic sclerosis: exploring cellular, genetic and epigenetic mechanisms.Rheumatology international · 2020Review
- Interplay between Cell-Surface Receptors and Extracellular Matrix in Skin.Biomolecules · 2020Review
- Cross-Talk between Transforming Growth Factor-β and Periostin Can Be Targeted for Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2020Article
- GIPC-Regulated IGFBP-3 Promotes HSC Migration In Vitro and Portal Hypertension In Vivo Through a β1-Integrin Pathway.Cellular and molecular gastroenterology and hepatology · 2020Article
- The Cardiac Syndecan-2 Interactome.Frontiers in cell and developmental biology · 2020Article
- Syndecan-4 Inhibits the Development of Pulmonary Fibrosis by Attenuating TGF-β Signaling.International journal of molecular sciences · 2019Article
- Interferon-γ enhances the antifibrotic effects of pirfenidone by attenuating IPF lung fibroblast activation and differentiation.Respiratory research · 2019Article
- Use of cholesterol and soluble tumour markers CEA and syndecan-2 in pleural effusions in cases of inconclusive cytology.Journal of clinical pathology · 2019Article
- Spotlight on the Transglutaminase 2-Heparan Sulfate Interaction.Medical sciences (Basel, Switzerland) · 2019Review
- Insulin-Like Growth Factor-1 Signaling in Lung Development and Inflammatory Lung Diseases.BioMed research international · 2018Review
- Matrix metalloproteinases as therapeutic targets for idiopathic pulmonary fibrosis.American journal of respiratory cell and molecular biology · 2015Review
- Syndecan-1 and Its Expanding List of Contacts.Advances in wound care · 2015Review
- Cellular interactions in the pathogenesis of interstitial lung diseases.European respiratory review : an official journal of the European Respiratory Society · 2015Review
- Similarities in Gene Expression Profiles during In Vitro Aging of Primary Human Embryonic Lung and Foreskin Fibroblasts.BioMed research international · 2015Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Extracellular matrix deposition and tissue scarring characterize the process of fibrosis. Transforming growth factor beta (TGFβ) and Insulin-like growth factor binding protein-3 (IGFBP-3) have been implicated in the pathogenesis of fibrosis in various tissues by inducing mesenchymal cell proliferation and extracellular matrix deposition. We identified Syndecan-2 (SDC2) as a gene induced by TGFβ in an IGFBP-3-dependent manner. TGFβ induction of SDC2 mRNA and protein required IGFBP-3. IGFBP-3 independently induced production of SDC2 in primary fibroblasts. Using an ex-vivo model of human skin in organ culture expressing IGFBP-3, we demonstrate that IGFBP-3 induces SDC2 ex vivo in human tissue. We also identified Mitogen-activated protein kinase-interacting kinase (Mknk2) as a gene induced by IGFBP-3. IGFBP-3 triggered Mknk2 phosphorylation resulting in its activation. Mknk2 independently induced SDC2 in human skin. Since IGFBP-3 is over-expressed in fibrotic tissues, we examined SDC2 levels in skin and lung tissues of patients with systemic sclerosis (SSc) and lung tissues of patients with idiopathic pulmonary fibrosis (IPF). SDC2 levels were increased in fibrotic dermal and lung tissues of patients with SSc and in lung tissues of patients with IPF. This is the first report describing elevated levels of SDC2 in fibrosis. Increased SDC2 expression is due, at least in part, to the activity of two pro-fibrotic factors, TGFβ and IGFBP-3.
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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.