ArticleArteriosclerosis, thrombosis, and vascular biology2009
Syndecan-1: an inhibitor of arterial smooth muscle cell growth and intimal hyperplasia.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 37 citations in OpenAlex.
- Deficiency of p27Journal of vascular research · 2026Article
- Circulating and Respiratory Biomarkers in Sepsis-Induced ARDS: Diagnostic and Prognostic Insights - A Narrative Review.Journal of inflammation research · 2026Review
- Comparison between vascular smooth muscle cells isolated from descending thoracic and abdominal aortas of mice in cell function, phenotype features, and gene expression.JVS-vascular science · 2026Article
- Syndecan-1 as a Biomarker for Cardiovascular Risk in Patients with Behçet's Disease.Archives of rheumatology · 2025Article
- Proteoglycans as Biomarkers of Medial Degeneration in Acute Stanford Type A Aortic Dissection.Reviews in cardiovascular medicine · 2025Review
- Syndecan-1 Is Overexpressed in Human Thoracic Aneurysm but Is Dispensable for the Disease Progression in a Mouse Model.Frontiers in cardiovascular medicine · 2022Article
- Syndecan-1 downregulates syndecan-4 expression by suppressing the ERK1/2 and p38 MAPK signaling pathways in cultured vascular endothelial cells.Biochemistry and biophysics reports · 2021Article
- It takes more than two to tango: mechanosignaling of the endothelial surface.Pflugers Archiv : European journal of physiology · 2020Review
- Growth factors with enhanced syndecan binding generate tonic signalling and promote tissue healing.Nature biomedical engineering · 2020Article
- TRAIL signals, extracellular matrix and vessel remodelling.Vascular biology (Bristol, England) · 2020Review
- Syndecan-1 Predicts Outcome in Patients with ST-Segment Elevation Infarction Independent from Infarct-related Myocardial Injury.Scientific reports · 2019Article
- Endothelial Glycocalyx as Biomarker for Cardiovascular Diseases: Mechanistic and Clinical Implications.Current heart failure reports · 2017Review
- PDGFRα signalling promotes fibrogenic responses in collagen-producing cells in Duchenne muscular dystrophy.The Journal of pathology · 2016Article
- Overcoming disease-induced growth factor resistance in therapeutic angiogenesis using recombinant co-receptors delivered by a liposomal system.Biomaterials · 2014Article
- Syndecan-1 regulates vascular smooth muscle cell phenotype.PloS one · 2014Article
- Reciprocal regulation of syndecan-2 and Notch signaling in vascular smooth muscle cells.The Journal of biological chemistry · 2012Article
- Inhibition of PDGF-B induction and cell growth by syndecan-1 involves the ubiquitin and SUMO-1 ligase, Topors.PloS one · 2012Article
- Molecular functions of syndecan-1 in disease.Matrix biology : journal of the International Society for Matrix Biology · 2012Review
- Heparan sulfate proteoglycans.Cold Spring Harbor perspectives in biology · 2011Review
- Changes in expression of proteoglycan core proteins and heparan sulfate enzymes in the developing and adult murine aorta.Journal of cardiovascular translational research · 2011Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
objectiveArterial injury induces smooth muscle cell (SMC) proliferation, migration, and intimal accumulation of cells and extracellular matrix. These processes are regulated by the administration of the glycosaminoglycans heparin and heparan sulfate, but little is known about the role of endogenous heparan sulfate proteoglycans in the vessel wall. We investigated the response to carotid injury of syndecan-1-null mice to assess the function of one of a conserved family of transmembrane heparan and chondroitin sulfate proteoglycans. METHODS AND
resultsSyndecan-1-null mice developed a large neointimal lesion after injury, whereas wild-type mice made little or none. This was accompanied by a significant increase in both medial and intimal SMC replication. Cultured syndecan-1-null SMCs showed a significant increase in proliferation in response to PDGF-BB, thrombin, FGF2, EGF, and serum. In response to thrombin, PDGF-BB, and serum syndecan-1-null SMCs expressed more PDGF-B chain message than did wild-type SMCs. Downregulation of PDGF-BB or PDGFRbeta inhibited thrombin-, PDGF-BB-, and serum-induced DNA synthesis in syndecan-1-null SMCs.
conclusionsThese results suggest the possibility that syndecan-1 may limit intimal thickening in injured arteries by suppressing SMC activation through inhibition of SMC PDGF-B chain expression and PDGFRbeta activation.
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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.