ArticleHeart and vessels2011
Effect of mini-tyrosyl-tRNA synthetase/mini-tryptophanyl-tRNA synthetase on ischemic angiogenesis in rats: proliferation and migration of endothelial cells.
Article in Heart and vessels, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
The trial behind it
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- Machine learning-based biomarker profile derived from 4210 serially measured proteins predicts clinical outcome of patients with heart failure.European heart journal. Digital health · 2023Article
- New Candidates for Biomarkers and Drug Targets of Ischemic Stroke-A First Dynamic LC-MS Human Serum Proteomic Study.Journal of clinical medicine · 2022Article
- The regulatory roles of aminoacyl-tRNA synthetase in cardiovascular disease.Molecular therapy. Nucleic acids · 2021Review
- Microporous Biodegradable Films Promote Therapeutic Angiogenesis.Advanced healthcare materials · 2020Article
- Matrix metalloproteinases inactivate the proinflammatory functions of secreted moonlighting tryptophanyl-tRNA synthetase.The Journal of biological chemistry · 2019Article
- Emerging mechanisms of aminoacyl-tRNA synthetase mutations in recessive and dominant human disease.Human molecular genetics · 2017Review
- VEGF, not VEGFR2, is associated with the angiogenesis effect of mini-TyrRS/mini-TrpRS in human umbilical vein endothelial cells in hypoxia.Cytotechnology · 2014Article
- Natural aminoacyl tRNA synthetase fragment enhances cardiac function after myocardial infarction.PloS one · 2014Article
- Real-time tracking of adipose tissue-derived stem cells with injectable scaffolds in the infarcted heart.Heart and vessels · 2013Article
- IDO inhibits a tryptophan sufficiency signal that stimulates mTOR: A novel IDO effector pathway targeted by D-1-methyl-tryptophan.Oncoimmunology · 2012Article
- Inhibition of mini-TyrRS-induced angiogenesis response in endothelial cells by VE-cadherin-dependent mini-TrpRS.Heart and vessels · 2012Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The purpose of this study was to determine the mechanism of mini-tyrosyl-tRNA synthetase/mini-tryptophanyl-tRNA synthetase (mini-TyrRS/mini-TrpRS) on ischemic angiogenesis in rats with acute myocardial infarction and proliferation, migration, potential signaling pathways of rat coronary venular endothelial cells (RCVECs). The effects of mini-TyrRS/mini-TrpRS on RCVECs proliferation were evaluated using the MTT colorimetric assay. Cell migration was assayed using a modified Boyden chamber technique. The potential involvement of Erk and PI3K signaling pathways was explored using selective chemical inhibitor or Western-blot analysis. Left coronary artery ligation was used to establish the model of acute myocardial infarction in rats (Sprague-Dawley male rats, 200-250 g, 2-3 months old), 20 μl of mini-TyrRS, mini-TrpRS, or PBS (vehicle) was injected subcutaneously every 12 h. The rats were randomly divided into four experimental groups: sham operated group; coronary artery ligation (CAL); CAL + mini-TyrRS (20 μl, twice daily, 600 μg kg(-1) day(-1)); and CAL + mini-TrpRS (20 μl, twice daily, 600 μg kg(-1) day(-1)). The experiment was carried out at four time points on the 3rd, 7th, 14th, and 28th day after ligation. To determine whether mini-TyrRS/mini-TrpRS affected the angiogenesis activity of rats with myocardial infarction, we measured the myocardial infarction size by TTC staining, and microvessel density (MVD) was determined by CD34 staining. The results show that proliferation and migration in RCVECs could be promoted by mini-TyrRS at concentrations of 1-100 μg/ml, and inhibited by mini-TrpRS. Phospho-PI3-kinase and Erk expression increased significantly when mini-TyrRS was added, but could be attenuated by mini-TrpRS. Compared to the CAL group, the myocardial infarction size of the mini-TyrRS group at the 3rd, 7th, 14th, and 28th day were decreased, while mini-TrpRS increased, but only in days 14 and 28 was there a significant difference. Except that, the microvessel density of RCVECs was promoted in mini-TyrRS group but inhibited in the mini-TrpRS group. These results indicated that angiogenesis could be either stimulated by mini-TyrRS or inhibited by mini-TrpRS.
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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.