ArticleThe American journal of pathology1998
Differing patterns of P-selectin expression in lung injury.
Article in The American journal of pathology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 31 citations in OpenAlex.
- Circulating adhesion molecules and subclinical interstitial lung disease: the Multi-Ethnic Study of Atherosclerosis.The European respiratory journal · 2019Article
- Baclofen, a GABABR agonist, ameliorates immune-complex mediated acute lung injury by modulating pro-inflammatory mediators.PloS one · 2015Article
- Evaluation of variants in the selectin genes in age-related macular degeneration.BMC medical genetics · 2011Article
- C5a-induced gene expression in human umbilical vein endothelial cells.The American journal of pathology · 2004Article
- Discovery of a potent nanoparticle P-selectin antagonist with anti-inflammatory effects in allergic airway disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2003Article
- Expression of vascular adhesion protein-1 in normal and inflamed mice lungs and normal human lungs.Virchows Archiv : an international journal of pathology · 2003Article
- P-selectin upregulation in bleomycin induced lung injury in rats: effect of N-acetyl-L-cysteine.Thorax · 2002Article
- Pressure is proinflammatory in lung venular capillaries.The Journal of clinical investigation · 1999Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
Using two models of acute lung inflammatory injury in rats (intrapulmonary deposition of immunoglobulin G immune complexes and systemic activation of complement after infusion of purified cobra venom factor), we have analyzed the requirements and patterns for upregulation of lung vascular P-selectin. In the immune complex model, upregulation of P-selectin was defined by Northern and Western blot analysis of lung homogenates, by immunostaining of lung tissue, and by vascular fixation of 125I-labeled anti-P-selectin. P-selectin protein was detected by 1 hour (long before detection of mRNA) and expression was sustained for the next 7 hours, in striking contrast to the pattern of P-selectin expression in the cobra venom factor model, in which upregulation was very transient (within the 1st hour). In the immune complex model, injury and neutrophil accumulation were P-selectin dependent. Upregulation of P-selectin was dependent on an intact complement system, and the presence of blood neutrophils was susceptible to the antioxidant dimethyl sulfoxide and required C5a but not tumor necrosis factor alpha. In contrast, in the cobra venom factor model, upregulation of P-selectin, which is C5a dependent, was also dimethyl sulfoxide sensitive but neutrophil independent. Different mechanisms that may explain why upregulation of lung vascular P-selectin is either transient or sustained are discussed.
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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.