ArticleThe Journal of cell biology2003
PMN transendothelial migration decreases nuclear NFkappaB in IL-1beta-activated endothelial cells: role of PECAM-1.
Article in The Journal of cell biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 46 citations in OpenAlex.
- Personalized risk predictor for acute cellular rejection in lung transplant using soluble CD31.Scientific reports · 2022Article
- Role and Potential Mechanism of Heme Oxygenase-1 in Intestinal Ischemia-Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2022Article
- The psychoactive drug of abuse mephedrone differentially disrupts blood-brain barrier properties.Journal of neuroinflammation · 2021Article
- Metabolic adaptations of cells at the vascular-immune interface during atherosclerosis.Molecular aspects of medicine · 2021Article
- Platelet Endothelial Cell Adhesion Molecule-1 and Oligodendrogenesis: Significance in Alcohol Use Disorders.Brain sciences · 2017Review
- Selective induction of cell adhesion molecules by proinflammatory mediators in human cardiac microvascular endothelial cells in culture.International journal of clinical and experimental medicine · 2010Article
- PECAM-1: conflicts of interest in inflammation.Life sciences · 2010Review
- Carbon monoxide liberated from CO-releasing molecule (CORM-2) attenuates ischemia/reperfusion (I/R)-induced inflammation in the small intestine.Inflammation · 2010Article
- The anti-inflammatory actions of platelet endothelial cell adhesion molecule-1 do not involve regulation of endothelial cell NF-kappa B.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Inflammatory response in microvascular endothelium in sepsis: role of oxidants.Journal of clinical biochemistry and nutrition · 2008Article
- Cell type-specific aspects in biocompatibility testing: the intercellular contact in vitro as an indicator for endothelial cell compatibility.Journal of materials science. Materials in medicine · 2008Article
- Detection of differentially expressed glycogenes in trabecular meshwork of eyes with primary open-angle glaucoma.Investigative ophthalmology & visual science · 2006Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During the systemic inflammatory response, circulating cytokines interact with the vascular endothelium, resulting in activation and nuclear accumulation of the nuclear transcription factor, nuclear factor kappa B (NFkappaB). In turn, NFkappaB transactivates relevant proinflammatory genes, resulting in an amplification of the inflammatory response. Because this scenario is potentially detrimental to the host, mechanisms exist to limit this amplification. Using an in vitro system that mimics the vascular-interstitial interface during inflammation (cell culture inserts), we provide evidence for the existence of a novel negative feedback mechanism on NFkappaB activity. We show that the interleukin 1beta-induced accumulation of nuclear NFkappaB in human umbilical vein endothelial cell monolayers is dramatically reduced when polymorphonuclear leukocytes (PMN) are allowed to migrate across these monolayers. This effect does not appear to be due to PMN-derived elastase or nitric oxide. Fixed PMN (adhere but do not migrate) did not affect nuclear NFkappaB. Furthermore, cross-linking of platelet-endothelial cell adhesion molecule-1 (PECAM-1), but not intercellular adhesion molecule-1, reduces human umbilical vein endothelial cell nuclear NFkappaB induced by interleukin 1beta. Finally, interaction of PMN with PECAM-1-deficient endothelial cells does not reduce nuclear NFkappaB. These observations indicate that engagement of PECAM-1 by emigrating PMN is a pivotal event in this negative feedback on NFkappaB activity.
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