ArticleThe Journal of biological chemistry2008
Syndecan-1 is an in vivo suppressor of Gram-positive toxic shock.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 46 citations in OpenAlex.
- Heparan Sulfate Proteoglycans in Immunity.Proteoglycan research · 2026Article
- Shed Syndecan-4 and Its Possible Roles in Osteoarthritis.Biomedicines · 2025Review
- Sequential Extracorporeal Therapy of Pathogen Removal Followed by Cell-Directed Extracorporeal Therapy in Streptococcal Toxic Shock Syndrome Refractory to Venoarterial Extracorporeal Membrane Oxygenation: A Case Report.Critical care explorations · 2024Article
- SEC is an antiangiogenic virulence factor that promotesScience advances · 2022Article
- Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage.Biomedicines · 2020Review
- Article
- Soluble syndecans: biomarkers for diseases and therapeutic options.British journal of pharmacology · 2019Review
- Network of Mediators for Vascular Inflammation and Leakage Is Dysbalanced during Cytoreductive Surgery for Late-Stage Ovarian Cancer.Mediators of inflammation · 2019Article
- Isolation and functional analysis of syndecans.Methods in cell biology · 2018Article
- Circulating Heparan Sulfate Fragments Attenuate Histone-Induced Lung Injury Independently of Histone Binding.Shock (Augusta, Ga.) · 2017Article
- Syndecan-1 limits the progression of liver injury and promotes liver repair in acetaminophen-induced liver injury in mice.Hepatology (Baltimore, Md.) · 2017Article
- Shock induced endotheliopathy (SHINE) in acute critical illness - a unifying pathophysiologic mechanism.Critical care (London, England) · 2017Review
- Syndecan-1 deficiency promotes tumor growth in a murine model of colitis-induced colon carcinoma.PloS one · 2017Article
- Glycosaminoglycans and infection.Frontiers in bioscience (Landmark edition) · 2016Review
- 2-O-Sulfated Domains in Syndecan-1 Heparan Sulfate Inhibit Neutrophil Cathelicidin and Promote Staphylococcus aureus Corneal Infection.The Journal of biological chemistry · 2015Article
- Syndecan-1 restitution by plasma after hemorrhagic shock.The journal of trauma and acute care surgery · 2015Review
- Article
- The endothelial glycocalyx in syndecan-1 deficient mice.Microvascular research · 2013Article
- Syndecan-1 displays a protective role in aortic aneurysm formation by modulating T cell-mediated responses.Arteriosclerosis, thrombosis, and vascular biology · 2012Article
- Shedding of cell membrane-bound proteoglycans.Methods in molecular biology (Clifton, N.J.) · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
Abstract
Heparan sulfate proteoglycans bind to and regulate many inflammatory mediators in vitro, suggesting that they serve an important role in influencing inflammatory responses in vivo. Here we evaluated the role of syndecan-1, a major heparan sulfate proteoglycan, in modulating inflammatory responses in Gram-positive toxic shock, a systemic disease that is a significant cause of morbidity and mortality. Syndecan-1-null and wild-type mice were injected intraperitoneally with staphylococcal enterotoxin B, a pyrogenic superantigen, and their inflammatory responses were assessed. Syndecan-1-null mice showed significantly increased liver injury, vascular permeability, and death in response to staphylococcal enterotoxin B challenge compared with wild-type mice. Although serum levels of systemic IL-2 and IFNgamma were similar between the two backgrounds, those of TNFalpha and IL-6 were significantly increased in syndecan-1-null mice undergoing Gram-positive toxic shock. Furthermore, syndecan-1-null mice challenged with staphylococcal enterotoxin B showed enhanced T cell accumulation in tissues, whereas immunodepletion of T cells protected syndecan-1-null mice from the magnified systemic cytokine storm, inflammatory tissue injury, and death. Importantly, syndecan-1 shedding was induced in wild-type mice injected with staphylococcal enterotoxin B, and the administration of heparan sulfate, but not syndecan-1 core protein, rescued syndecan-1-null mice from lethal toxic shock by suppressing the production of TNFalpha and IL-6, and attenuating inflammatory tissue injury. Altogether, these data suggest that syndecan-1 shedding is a key endogenous mechanism that protects the host from Gram-positive toxic shock by inhibiting the dysregulation and amplification of the inflammatory response.
Indexed as
Identifiers
What OpenQuestion holds
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.