ArticleAmerican journal of respiratory and critical care medicine2016
Syndecan-1 Attenuates Lung Injury during Influenza Infection by Potentiating c-Met Signaling to Suppress Epithelial Apoptosis.
Article in American journal of respiratory and critical care medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 60 citations in OpenAlex.
- Syndecan-1 Promotes Alveolar Type 2 Epithelial Cell Senescence during Lung Fibrosis.bioRxiv : the preprint server for biology · 2026Article
- From Alveolar Injury to Precision Perioperative Care: Integrating Molecular Biomarkers and Technology-Enabled Strategies for Prolonged Air Leak After Lung Resection.Mediators of inflammation · 2026Review
- The LTB4-BLT1 axis attenuates influenza-induced lung inflammation by suppressing NLRP3 activation.Cell death discovery · 2025Article
- c-Met inhibitor NVP-BVU972 induces antiviral protection and suppresses NF-κB-mediated inflammation.Frontiers in immunology · 2025Article
- Cellular Mechanisms of Lung Injury: Current Perspectives.Clinics in chest medicine · 2024Review
- Antibiotic use during influenza infection augments lung eosinophils that impair immunity against secondary bacterial pneumonia.The Journal of clinical investigation · 2024Article
- Investigating the effects ofHeliyon · 2024Article
- Interstitial Macrophages Mediate Efferocytosis of Alveolar Epithelium during Influenza Infection.American journal of respiratory cell and molecular biology · 2024Article
- Assessment of MMP-9 and clinical characteristics in dogs with tracheal collapse based on cough severity and fluoroscopic findings: a cross-sectional study.BMC veterinary research · 2024Article
- Matrix metalloproteinases mediate influenza A-associated shedding of the alveolar epithelial glycocalyx.PloS one · 2024Article
- The role of the alveolar epithelial glycocalyx in acute respiratory distress syndrome.American journal of physiology. Cell physiology · 2023Review
- Protectin DX Relieve Hyperoxia-induced Lung Injury by Protecting Pulmonary Endothelial Glycocalyx.Journal of inflammation research · 2023Article
- New Insights into the Alveolar Epithelium as a Driver of Acute Respiratory Distress Syndrome.Biomolecules · 2022Review
- Heparan Sulfate and Sialic Acid in Viral Attachment: Two Sides of the Same Coin?International journal of molecular sciences · 2022Review
- IL-34 and protein-tyrosine phosphatase receptor type-zeta-dependent mechanisms limit arthritis in mice.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Extracellular vesicles in idiopathic pulmonary fibrosis: pathogenesis and therapeutics.Inflammation and regeneration · 2022Review
- The host response in different aetiologies of community-acquired pneumonia.EBioMedicine · 2022Article
- Indications of Persistent Glycocalyx Damage in Convalescent COVID-19 Patients: A Prospective Multicenter Study and Hypothesis.Viruses · 2021Observational
- Targeting highly pathogenic coronavirus-induced apoptosis reduces viral pathogenesis and disease severity.Science advances · 2021Article
- Extracellular Vesicles: Versatile Nanomediators, Potential Biomarkers and Therapeutic Agents in Atherosclerosis and COVID-19-Related Thrombosis.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
rationaleSyndecan-1 is a cell surface heparan sulfate proteoglycan primarily expressed in the lung epithelium. Because the influenza virus is tropic to the airway epithelium, we investigated the role of syndecan-1 in influenza infection.
objectivesTo determine the mechanism by which syndecan-1 regulates the lung mucosal response to influenza infection.
methodsWild-type (WT) and Sdc1(-/-) mice were infected with a H1N1 virus (PR8) as an experimental model of influenza infection. Human and murine airway epithelial cell cultures were also infected with PR8 to study the mechanism by which syndecan-1 regulates the inflammatory response. MEASUREMENT AND MAIN
resultsWe found worsened outcomes and lung injury in Sdc1(-/-) mice compared with WT mice after influenza infection. Our data demonstrated that syndecan-1 suppresses bronchial epithelial apoptosis during influenza infection to limit widespread lung inflammation. Furthermore, we determined that syndecan-1 attenuated apoptosis by crosstalking with c-Met to potentiate its cytoprotective signals in airway epithelial cells during influenza infection.
conclusionsOur work shows that cell-associated syndecan-1 has an important role in regulating lung injury. Our findings demonstrate a novel mechanism in which cell membrane-associated syndecan-1 regulates the innate immune response to influenza infection by facilitating cytoprotective signals through c-Met signaling to limit bronchial epithelial apoptosis, thereby attenuating lung injury and inflammation.
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