ArticleThe Journal of experimental medicine1999
Essential role of P-selectin in the initiation of the inflammatory response induced by hemorrhage and reinfusion.
Article in The Journal of experimental medicine, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
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.
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Who cites it
19 citing papers in PubMed, 82 citations in OpenAlex.
- Trial
- Platelets as Central Modulators of Post-Cardiac Arrest Syndrome: Mechanisms and Therapeutic Implications.Biomolecules · 2026Review
- Molecular mechanisms of catch bonds and their implications for platelet hemostasis.Biophysical reviews · 2023Review
- Dual phenotypic characteristics of P-selectin in a mouse model of hemorrhagic shock and hepatectomy.Heliyon · 2023Article
- Novel Strategies for Endothelial Preservation in Lung Transplant Ischemia-Reperfusion Injury.Frontiers in physiology · 2020Review
- Improvement of core-fucosylated glycoproteome coverage via alternating HCD and ETD fragmentation.Journal of proteomics · 2016Article
- Carbon monoxide protects against hemorrhagic shock and resuscitation-induced microcirculatory injury and tissue injury.Shock (Augusta, Ga.) · 2015Article
- Inhibition of Rho-kinase attenuates endothelial-leukocyte interaction during ischemia-reperfusion injury.Vascular medicine (London, England) · 2012Article
- A reversible aptamer improves outcome and safety in murine models of stroke and hemorrhage.Oligonucleotides · 2011Article
- Targeting selectins and selectin ligands in inflammation and cancer.Expert opinion on therapeutic targets · 2007Review
- Evolutionary conservation of P-selectin glycoprotein ligand-1 primary structure and function.BMC evolutionary biology · 2007Article
- Adiponectin deficiency increases leukocyte-endothelium interactions via upregulation of endothelial cell adhesion molecules in vivo.The Journal of clinical investigation · 2007Article
- Clinical peritoneal dialysis solutions modulate white blood cell-intestinal vascular endothelium interaction.American journal of surgery · 2006Article
- Inhibition of Rho-kinase leads to rapid activation of phosphatidylinositol 3-kinase/protein kinase Akt and cardiovascular protection.Arteriosclerosis, thrombosis, and vascular biology · 2004Article
- Important role of P-selectin for leukocyte recruitment, hepatocellular injury, and apoptosis in endotoxemic mice.Clinical and diagnostic laboratory immunology · 2004Article
- Relative contributions of selectins and intercellular adhesion molecule-1 to tissue injury induced by immune complex deposition.The American journal of pathology · 2003Article
- Cell adhesion molecules involved in the leukocyte recruitment induced by venom of the snake Bothrops jararaca.Mediators of inflammation · 2002Article
- Effect of N-desulfated heparin on hepatic/renal ischemia reperfusion injury in rats.World journal of gastroenterology · 2002Article
- N-acetylcysteine induces shedding of selectins from liver and intestine during orthotopic liver transplantation.Clinical and experimental immunology · 2001Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Resuscitation from hemorrhage induces profound pathophysiologic alterations and activates inflammatory cascades able to initiate neutrophil accumulation in a variety of tissues. This process is accompanied by acute organ damage (e.g., lungs and liver). We have previously demonstrated that significant leukocyte-endothelium interactions occur very early in other forms of ischemia/reperfusion (i.e., splanchnic ischemia/reperfusion and traumatic shock) which are largely mediated by increased expression of the adhesion molecule, P-selectin, on the vascular endothelium. Here we postulated that increased endothelial expression of P-selectin in the microvasculature would play an essential role in initiating the inflammatory signaling of hemorrhagic shock. Using intravital microscopy, we found that hemorrhagic shock significantly increased the number of rolling and adherent leukocytes in the mouse splanchnic microcirculation. In contrast, mice genetically deficient in P-selectin, or wild-type mice given either an anti-P-selectin monoclonal antibody or a recombinant soluble P-selectin glycoprotein ligand (PSGL)-1 immunoglobulin, exhibited markedly attenuated leukocyte-endothelium interaction after hemorrhagic shock. Thus, activation of P-selectin protein on the microvascular endothelium is essential for the initial upregulation of the inflammatory response occurring in hemorrhagic shock. Moreover, endogenous levels of PSGL-1 mRNA were significantly increased in the lung, liver, and small intestine of wild-type mice subjected to hemorrhagic shock. Since PSGL-1 promotes adhesive interactions largely through P-selectin expressed on the vascular endothelium, this result further supports the crucial role played by P-selectin in the recruitment of leukocytes during hemorrhagic shock.
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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.