ArticleMicrocirculation (New York, N.Y. : 1994)2014
Homocysteine disrupts outgrowth of microvascular endothelium by an iNOS-dependent mechanism.
Article in Microcirculation (New York, N.Y. : 1994), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
3 citing papers in PubMed.
- Article
- Calcium and electrical signaling in arterial endothelial tubes: New insights into cellular physiology and cardiovascular function.Microcirculation (New York, N.Y. : 1994) · 2017Review
- The connexin 43/ZO-1 complex regulates cerebral endothelial F-actin architecture and migration.American journal of physiology. Cell physiology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
objectiveTo test the hypothesis that Hcy impairs angiogenic outgrowth through an iNOS-dependent mechanism.
methodsAdult C57Bl/6 mouse choroid explants were used in angiogenic outgrowth assays. Mouse microvascular endothelial cells were studied in culture during scrape-induced migration and dispersed cell locomotion experiments. Activity of iNOS was manipulated with pharmacology (1400 W), siRNA, and by use of choroid explants from iNOS knockout mice (iNOS(-/-)).
resultsHcy (20 μM) significantly decreased the area of endothelial outgrowth without altering the number of cells in the choroid explant angiogenic assay, resulting in more densely packed outgrowth. Hcy prevented the outward orientation of actin filaments and decreased the number of actin projections along the leading edge of outgrowth. Hcy also slowed outgrowth from the edge of a scraped endothelial monolayer and in cultures of dispersed cells, Hcy impaired cell locomotion without affecting proliferation. Inhibition of iNOS activity rescued the effect of Hcy on area of explant outgrowth, cell density, number of projections, cell locomotion, and rate of outgrowth following scraping.
conclusionsHcy impairs microvascular endothelial outgrowth, but not proliferation, by disrupting cell locomotion through an iNOS-dependent mechanism.
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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.