ArticleAgents and actions1994
Lectin-induced increase in microvascular permeability to colloidal carbon in vitro may involve protein kinase C activation.
Article in Agents and actions, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Role of Mast Cells and C-Sensory Fibers in Concanavalin A-Induced Paw Edema in Two Rat Strains.Inflammation · 2015Article
- Crystallization and characterization of an inflammatory lectin purified from the seeds of Dioclea wilsonii.Molecules (Basel, Switzerland) · 2011Article
- Vasodilator effects of Diocleinae lectins from the Canavalia genus.Naunyn-Schmiedeberg's archives of pharmacology · 2009Article
- Rate of perfusion modulates colloidal carbon leakage from rat intestinal microvessels in vitro.Mediators of inflammation · 1995Article
- Vasoconstriction in rat isolated mesentery and small intestine in response to various activators of protein kinase C.Agents and actions · 1994Article
- Stimulation of protein kinase C activity may increase microvascular permeability to colloidal carbon via alpha-isoenzyme.Inflammation · 1994Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Two plant lectins, wheat germ agglutinin (WGA) and concanavalin A (Con A), which are known to bind to endothelial cells (ECs), were found to increase the leakage of colloidal carbon (CC) into the walls of microvessels in the villi of rat small intestine, when added to a gelatin-containing perfusate (GPSS) at a concentration of 10 micrograms/ml. Pretreatment of the microvessels with the protein kinase C (PKC) inhibitor Ro 31-8220 (1 x 10(-6) M) significantly reduced this effect. In contrast, the leakage of CC in response to A23187 (1 x 10(-4) M) was not affected by Ro 31-8220. Peanut agglutinin (PNA) and succinyl concanavalin A (SuccCon A), which do not bind to ECs, had no effect at a concentration of 10 micrograms/ml. A lower concentration of WGA (1 microgram/ml) had no significant effect of its own, but significantly reduced the leakage of CC in response to both platelet-activating factor (PAF, 5 x 10(-6) M) and 5-hydroxytryptamine (5-HT, 1 x 10(-4) M), but not to beta-phorbol 12,13-dibutyrate (PDB, 1 x 10(-6) M). These results suggest that all these effects of WGA and Con A involve cell surface receptors, albeit in a non-specific way. A possible mode of action is discussed.
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