ArticleArteriosclerosis, thrombosis, and vascular biology2012
Syndecan-1 displays a protective role in aortic aneurysm formation by modulating T cell-mediated responses.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 37 citations in OpenAlex.
- A CD138+ tumor-associated macrophage/Siglec-F+ neutrophil feed-forward loop promotes immune evasion in pancreatic cancer.The Journal of clinical investigation · 2026Article
- Macrophage-derived CCL20 promotes abdominal aortic aneurysm progression via lymphocytes CCR6.Frontiers in immunology · 2026Article
- Proteoglycans as Biomarkers of Medial Degeneration in Acute Stanford Type A Aortic Dissection.Reviews in cardiovascular medicine · 2025Review
- Transport across the thoracic aortic wall: implications for aneurysm pathobiology, diagnosis, and treatment.American journal of physiology. Heart and circulatory physiology · 2025Review
- A Narrative Review: Syndecans in Aortic Aneurysm Pathogenesis and Course-Biomarkers and Targets?International journal of molecular sciences · 2025Review
- Aortic Aneurysm: Finding the Right Target.Biomedicines · 2023Article
- Aortic aneurysms and markers of platelet activation, hemostasis, and endothelial disruption in people living with HIV.Frontiers in immunology · 2023Article
- Twenty Years of Studying AngII (Angiotensin II)-Induced Abdominal Aortic Pathologies in Mice: Continuing Questions and Challenges to Provide Insight Into the Human Disease.Arteriosclerosis, thrombosis, and vascular biology · 2022Review
- Interleukin-34-regulated T-cell responses in rheumatoid arthritis.Frontiers in medicine · 2022Review
- Syndecan-1 Is Overexpressed in Human Thoracic Aneurysm but Is Dispensable for the Disease Progression in a Mouse Model.Frontiers in cardiovascular medicine · 2022Article
- A reduction in the vascular smooth muscle cell focal adhesion component syndecan-4 is associated with abdominal aortic aneurysm formation.Clinical and translational medicine · 2021Article
- Syndecan-1 Expression Is Increased in the Aortic Wall of Patients with Type 2 Diabetes but Is Unrelated to Elevated Fasting Plasma Glucagon-Like Peptide-1.Biomedicines · 2021Article
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- M2 Macrophages as a Potential Target for Antiatherosclerosis Treatment.Neural plasticity · 2019Review
- Comparative gene array analyses of severe elastic fiber defects in late embryonic and newborn mouse aorta.Physiological genomics · 2018Article
- The heparan sulfate proteoglycan grip on hyperlipidemia and atherosclerosis.Matrix biology : journal of the International Society for Matrix Biology · 2018Review
- Abdominal Aortic Aneurysm: Evolving Controversies and Uncertainties.The International journal of angiology : official publication of the International College of Angiology, Inc · 2018Review
- Inhibition or deletion of angiotensin II type 1 receptor suppresses elastase-induced experimental abdominal aortic aneurysms.Journal of vascular surgery · 2018Article
- A Novel Subset of Anti-Inflammatory CD138Journal of immunology (Baltimore, Md. : 1950) · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveChronic inflammation drives progressive and pathological remodeling inherent to formation of abdominal aortic aneurysm (AAA). Syndecan-1 (Sdc-1) is a cell surface heparan sulfate proteoglycan that displays the capacity to modulate inflammatory processes within the vascular wall. In the current investigation, the role of Sdc-1 in AAA formation was examined using 2 models of experimental aneurysm induction, angiotensin II infusion and elastase perfusion. METHODS AND
resultsSdc-1 deficiency exacerbated AAA formation in both experimental models and was associated with increased degradation of elastin, greater protease activity, and enhanced inflammatory cell recruitment into the aortic wall. Bone marrow transplantation studies indicated that deficiency of Sdc-1 in marrow-derived cells significantly contributed to AAA severity. Immunostaining revealed augmented Sdc-1 expression in a subset of AAA localized macrophages. We specifically characterized a higher percentage of CD4(+) T cells in Sdc-1-deficient AAA, and antibody depletion studies established the active role of T cells in aneurysmal dilatation. Finally, we confirmed the ability of Sdc-1 macrophage to modulate the inflammatory chemokine environment.
conclusionsThese investigations identify cross-talk between Sdc-1-expressing macrophages and AAA-localized CD4(+) T cells, with Sdc-1 providing an important counterbalance to T-cell-driven inflammation in the vascular wall.
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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.