ArticleInflammation2002
Inhibition of prostaglandin G/H synthase unveils a potent effect of platelet activating factor on the permeability of bovine aortic endothelial cells to albumin.
Article in Inflammation, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed, 5 citations in OpenAlex.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Platelet Activating Factor (PAF) is a very potent stimulant of various cell functions but little is known about the mechanisms responsible for its marked effect on endothelial permeability. An in vitro assay system was used to assess the direct effect of PAF on the permeability of a bovine aortic endothelial cell (BAEC) monolayer to albumin. PAF produced a small but not significant increase of the permeability of BAEC monolayer to albumin. However, pre-treatment of the monolayer with indomethacin (10 microM) resulted in a significant increase of BAEC permeability following PAF administration. This increase was concentration-dependent up to a maximal effect of 105% above basal value (for 0.1 microM PAF). Addition of the PAF antagonist SRI 63 441ZI (5 microM) abolished this effect. Exogenous administration of PGE2 (10(-7) M) inhibited the effect of PAF on the BAEC permeability suggesting that prostaglandins synthesized by the endothelium behave as a negative autoregulatory factor. Compound SRI 63 441ZI also partially inhibited bradykinin-induced permeability to albumin but did not significantly modify the activity of thrombin. These findings show that PAF can increase endothelial permeability to albumin when the synthesis of prostaglandins is inhibited. Our results also show that PAF might have an autocrine activity by mediating part of BK-induced permeability.
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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.