ArticleThe Journal of biological chemistry2014
Loss of syndecan-1 induces a pro-inflammatory phenotype in endothelial cells with a dysregulated response to atheroprotective flow.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
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Who cites it
82 citing papers in PubMed, 129 citations in OpenAlex.
- Article
- Biomarkers and Endothelial Damage in Obesity: An Insight into the Pharmacological Modulation.International journal of molecular sciences · 2026Review
- Return to an extreme environment exposure after pulmonary infection: SCUBA diving as a model?Physiological reports · 2026Article
- Role of neutrophils in regulating vascular permeability in inflammatory and autoimmune diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Multimodal Profiling Reveals Distinct Endothelial Activation Pathways Regulated by Flow and Heparan Sulfate.Cellular and molecular bioengineering · 2026Article
- Heparan Sulfates Regulate Vascular Reactivity in Syndecan 1 Knockout Mice.International journal of molecular sciences · 2026Article
- Mechanoresponsive ion channels Piezo1 and TRPV4 stimulate ADAM10 and ADAM17 with differential impact on endothelial migration and proliferation.Cell communication and signaling : CCS · 2026Article
- Serum Syndecan-1: a potent prognostic biomarker for transplant outcomes.Frontiers in medicine · 2026Article
- Unfractionated Heparin Attenuates Histone-Induced Pulmonary Endothelial Glycocalyx Injury: A Preliminary Study on the Roles of the ROCK Pathway and Heparanase‑1.Journal of inflammation research · 2026Article
- The glycocalyx: a key target for treatment of severe acute pancreatitis-associated multiple organ dysfunction syndrome.Human cell · 2025Review
- Modular cone-and-plate device for mechanofluidic assays in Transwell inserts.Frontiers in bioengineering and biotechnology · 2025Article
- Integrating molecular and cellular components of endothelial shear stress mechanotransduction.American journal of physiology. Heart and circulatory physiology · 2024Review
- Extracellular Matrix Components and Mechanosensing Pathways in Health and Disease.Biomolecules · 2024Review
- Syndecan-1 Levels in Females with Active Rheumatoid Arthritis.Journal of clinical medicine · 2024Article
- Control of tissue homeostasis by the extracellular matrix: Synthetic heparan sulfate as a promising therapeutic for periodontal health and bone regeneration.Periodontology 2000 · 2024Review
- Dysregulated complement activation during acute myocardial infarction leads to endothelial glycocalyx degradation and endothelial dysfunction via the C5a:C5a-Receptor1 axis.Frontiers in immunology · 2024Article
- Endocan, a novel glycoprotein with multiple biological activities, may play important roles in neurological diseases.Frontiers in aging neuroscience · 2024Review
- High salt intake and HIV infection on endothelial glycocalyx shedding in salt-sensitive hypertension.Frontiers in cell and developmental biology · 2024Review
- Capillary leak and endothelial permeability in critically ill patients: a current overview.Intensive care medicine experimental · 2023Review
- Neuraminidase inhibition improves endothelial function in diabetic mice.American journal of physiology. Heart and circulatory physiology · 2023Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Fluid shear stresses are potent regulators of vascular homeostasis and powerful determinants of vascular disease progression. The glycocalyx is a layer of glycoaminoglycans, proteoglycans, and glycoproteins that lines the luminal surface of arteries. The glycocalyx interacts directly with hemodynamic forces from blood flow and, consequently, is a prime candidate for the mechanosensing of fluidic shear stresses. Here, we investigated the role of the glycocalyx component syndecan-1 (sdc-1) in controlling the shear stress-induced signaling and flow-mediated phenotypic modulation in endothelial cells. We found that knock-out of sdc-1 abolished several key early signaling events of endothelial cells in response to shear stress including the phosphorylation of Akt, the formation of a spatial gradient in paxillin phosphorylation, and the activation of RhoA. After exposure to atheroprotective flow, we found that sdc-1 knock-out endothelial cells had a phenotypic shift to an inflammatory/pro-atherosclerotic phenotype in contrast to the atheroprotective phenotype of wild type cells. Consistent with these findings, we found increased leukocyte adhesion to sdc-1 knock-out endothelial cells in vitro that was reduced by re-expression of sdc-1. In vivo, we found increased leukocyte recruitment and vascular permeability/inflammation in sdc-1 knock-out mice. Taken together, our studies support a key role for sdc-1 in endothelial mechanosensing and regulation of endothelial phenotype.
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