ArticleInflammation1995
Protein kinase C inhibitor calphostin C prevents cytokine-induced angiogenesis in the rat.
Article in Inflammation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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
2 citing papers in PubMed, 22 citations in OpenAlex.
- Interplay between FAK, PKCδ, and p190RhoGAP in the regulation of endothelial barrier function.Microvascular research · 2012Review
- Comparative studies of the angiogenic activity of vasoactive intestinal peptide, endothelins-1 and -3 and angiotensin II in a rat sponge model.British journal of pharmacology · 1996Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
A rat sponge implant model was used to examine the role of protein kinase C (PKC) in angiogenesis. Neovascular response was determined by measurements of relative sponge blood flow by a 133Xe clearance technique and confirmed histologically. Morphometric analysis was used to quantitate the amount of fibrovascular growth in the sponges. Daily doses of recombinant human basic fibroblast growth factor (bFGF, 100 ng), tumor necrosis factor-alpha (TNF-alpha, 50 ng), or interleukin-1-alpha (IL-1 alpha, 50 ng) caused neovascular responses that were blocked by daily coadministration of the selective PKC inhibitor, calphostin C (4 micrograms). To confirm that calphostin C was able to inhibit PKC in vivo, its effect on the angiogenic response elicited by the PKC activator, phorbol 12-myristate 13-acetate (PMA, 30 micrograms) was examined. The blood flow and morphometric data clearly showed that the intense neovascularization induced by PMA was totally suppressed by coadministration of calphostin C (4 micrograms). Thus, these results suggest that cytokine-induced angiogenesis may be mediated in part through the activation of PKC and that selective inhibition of this enzyme could have therapeutic benefit in angiogenic diseases.
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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.