ArticleHeart and vessels2012
Inhibition of mini-TyrRS-induced angiogenesis response in endothelial cells by VE-cadherin-dependent mini-TrpRS.
Article in Heart and vessels, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- The high-affinity tryptophan uptake transport system in human cells.Biochemical Society transactions · 2024Review
- The regulatory roles of aminoacyl-tRNA synthetase in cardiovascular disease.Molecular therapy. Nucleic acids · 2021Review
- Aminoacyl-tRNA synthetases as therapeutic targets.Nature reviews. Drug discovery · 2019Review
- An alternative conformation of human TrpRS suggests a role of zinc in activating non-enzymatic function.RNA biology · 2018Article
- Emerging mechanisms of aminoacyl-tRNA synthetase mutations in recessive and dominant human disease.Human molecular genetics · 2017Review
- Identification of a residue crucial for the angiostatic activity of human mini tryptophanyl-tRNA synthetase by focusing on its molecular evolution.Scientific reports · 2016Article
- Cardioprotective effects of adipokine apelin on myocardial infarction.Heart and vessels · 2014Article
- VEGF, not VEGFR2, is associated with the angiogenesis effect of mini-TyrRS/mini-TrpRS in human umbilical vein endothelial cells in hypoxia.Cytotechnology · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To clarify whether a VE-cadherin-dependent pathway allows mini-TrpRS to inhibit mini-TrpRS-induced new blood vessel formation in endothelial cells (ECs), the inhibitory effects of mutant mini-TrpRS and VE-cadherin on mini-TrpRS-induced angiogenesis were investigated. The effects of mini-TyrRS and mini-TrpRS on EC proliferation were evaluated using an MTT colorimetric assay. Cell migration was assayed using a modified Boyden chamber technique. The angiogenic activity in vitro was evaluated by transwell migration assay and matrigel-induced capillary tube formation. It was found that mini-TrpRS does not inhibit the mini-TyrRS-induced proliferation and migration of EC under the condition of VE-cadherin knockout. While wild-type mini-TrpRS inhibited mini-TyrRS-induced angiogenesis, this activity vanished for the mutant protein. Also, the promotion of angiogenesis by mini-TyrRS and the inhibition of angiogenesis by mini-TrpRS were VEGFR2 dependent but not VEGF dependent. Mini-TyrRS was able to increase the protein expression of VEGFR-2 in the presence of VE-cadherin, while no stimulatory effect of mini-TyrRS was detected when VE-cadherin was not present. Angiogenesis is therefore stimulated by mini-TyrRS and inhibited by mini-TrpRS, raising the possibility that mini-TyrRS and mini-TrpRS stimulate a common downstream signaling event: VE-cadherin. Thus, naturally occurring fragments of the two proteins involved in translation, TyrRS and TrpRS, have opposing activities on angiogenesis. The opposing activities of the two tRNA synthetases suggest tight regulation of the balance between pro- and antiangiogenic stimuli.
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