ArticleThe Biochemical journal1989
Bradykinin and thrombin effects on polyphosphoinositide hydrolysis and prostacyclin production in endothelial cells.
Article in The Biochemical journal, 1989. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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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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
4 citing papers in PubMed, 39 citations in OpenAlex.
- Thrombin promotes actin polymerization in U937 human monocyte-macrophage cells. Analysis of the signalling mechanisms mediating actin polymerization.The Biochemical journal · 1992Article
- Endothelial cell spreading on fibrin requires fibrinopeptide B cleavage and amino acid residues 15-42 of the beta chain.The Journal of clinical investigation · 1992Article
- Metabolism of inositol phosphates in ATP-stimulated vascular endothelial cells.The Biochemical journal · 1991Article
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostacyclin (PGI2) production by thrombin- and bradykinin-stimulated bovine aortic endothelial cells (BAEC) and human umbilical vein endothelial cells (HUVEC) was related to the receptor-linked activation of inositide hydrolysis. Bradykinin caused a rapid and transient 3-fold increase in the formation of inositol polyphosphates in BAEC. The increase in InsP3 reflected changes mainly in the Ins(1,4,5)P3 isomer. Thrombin was less effective than bradykinin in increasing InsP3 levels and appeared to only minimally stimulate the production of PGI2 in BAEC. In HUVEC, thrombin caused a 5-fold elevation of Ins(1,4,5)P3, closely related to a rise in PGI2 production. However, bradykinin did not affect inositol phosphates and PGI2 production in HUVEC. Other inositol phosphates were also assessed to obtain information on putative metabolism of Ins(1,4,5)P3. The present study supports the notion that formation of Ins(1,4,5)P3 is linked to an increase in PGI2 production in endothelial cells and furthermore provides evidence for a large degree of heterogeneity in the responses of BAEC and HUVEC to thrombin and bradykinin.
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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.