Effect of Mini‐Tyrosyl‐tRNA Synthetase/Mini‐Tryptophanyl‐tRNA Synthetase on Angiogenesis in Rhesus Monkeys after Acute Myocardial Infarction

Zeng, Rui; Wang, Mian; You, Gui ying; Yue, Rong zheng; Chen, Yu cheng; Zeng, Zhi; Li, Rui; Ou, Qiang; Zhang, Li

doi:10.1111/1755-5922.12161

Cited by 8 publications

(3 citation statements)

References 33 publications

(52 reference statements)

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“…Forward genetic screens conducted in zebrafish have linked iars1, sars1, and tars1 variants to defects in angiogenesis during development, which can also be induced through morpholino knockdown of the respective genes ( Jin et al, 2007 ; Fukui et al, 2009 ; Herzog et al, 2009 ; Cao et al, 2016 ; Castranova et al, 2016 ; Wang K et al, 2018 ), but not through general inhibition of protein synthesis ( Fukui et al, 2009 ; Herzog et al, 2009 ; Xu et al, 2012 ; Cao et al, 2016 ). Pro- and anti-angiogenic effects of TyrRS and TrpRS splice variants via the phosphoinositide 3-kinase (PI3K) and extracellular signal-regulated kinase (ERK) pathways have also been demonstrated in vivo in rats and rhesus monkeys ( Wang et al, 2016 ; Zeng et al, 2016 ). Additionally, a Wars2 variant identified through linkage analysis impairs cardiac angiogenesis in rats, and wars2 knockdown in zebrafish causes similar vascularization defects ( Wang et al, 2016 ).…”

Section: Animal Model Systems For Studying Recessive Ars Diseasesmentioning

confidence: 99%

“…Pro-and anti-angiogenic effects of TyrRS and TrpRS splice variants via the phosphoinositide 10. 3389/fnins.2023.1182874 Frontiers in Neuroscience 12 frontiersin.org 3-kinase (PI3K) and extracellular signal-regulated kinase (ERK) pathways have also been demonstrated in vivo in rats and rhesus monkeys (Wang et al, 2016;Zeng et al, 2016). Additionally, a Wars2 variant identified through linkage analysis impairs cardiac angiogenesis in rats, and wars2 knockdown in zebrafish causes similar vascularization defects (Wang et al, 2016).…”

Section: Animal Models To Investigate Secondary Ars Functionsmentioning

confidence: 99%

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Recessive aminoacyl-tRNA synthetase disorders: lessons learned from in vivo disease models

et al. 2023

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Protein synthesis is a fundamental process that underpins almost every aspect of cellular functioning. Intriguingly, despite their common function, recessive mutations in aminoacyl-tRNA synthetases (ARSs), the family of enzymes that pair tRNA molecules with amino acids prior to translation on the ribosome, cause a diverse range of multi-system disorders that affect specific groups of tissues. Neurological development is impaired in most ARS-associated disorders. In addition to central nervous system defects, diseases caused by recessive mutations in cytosolic ARSs commonly affect the liver and lungs. Patients with biallelic mutations in mitochondrial ARSs often present with encephalopathies, with variable involvement of peripheral systems. Many of these disorders cause severe disability, and as understanding of their pathogenesis is currently limited, there are no effective treatments available. To address this, accurate in vivo models for most of the recessive ARS diseases are urgently needed. Here, we discuss approaches that have been taken to model recessive ARS diseases in vivo, highlighting some of the challenges that have arisen in this process, as well as key results obtained from these models. Further development and refinement of animal models is essential to facilitate a better understanding of the pathophysiology underlying recessive ARS diseases, and ultimately to enable development and testing of effective therapies.

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Section: Animal Model Systems For Studying Recessive Ars Diseasesmentioning

confidence: 99%

Section: Animal Models To Investigate Secondary Ars Functionsmentioning

confidence: 99%

Recessive aminoacyl-tRNA synthetase disorders: lessons learned from in vivo disease models

et al. 2023

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“…Our findings showed that the level of this protein decreases in the acute phase of ischemic stroke. It is commonly observed that at the same conditions there is an increased expression of another form of this enzyme, mini-TrpRS, which impairs myocardial perfusion after infarction in rat [75] and in monkeys [76]. As an antagonist of ocular angiogenesis, it may also have a beneficial effect in inhibiting pathological neovascularization [77].…”

Section: Proteomics Analysismentioning

confidence: 99%

New Candidates for Biomarkers and Drug Targets of Ischemic Stroke—A First Dynamic LC-MS Human Serum Proteomic Study

Turek-Jakubowska¹,

Dębski

Jakubowski

et al. 2022

JCM

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(1) Background: The aim of this dynamic-LC/MS-human-serum-proteomic-study was to identify potential proteins-candidates for biomarkers of acute ischemic stroke, their changes during acute phase of stroke and to define potential novel drug-targets. (2) Methods: A total of 32 patients (29–80 years) with acute ischemic stroke were enrolled to the study. The control group constituted 29 demographically-matched volunteers. Subjects with stroke presented clinical symptoms lasting no longer than 24 h, confirmed by neurological-examination and/or new cerebral ischemia visualized in the CT scans (computed tomography). The analysis of plasma proteome was performed using LC-MS (liquid chromatography–mass spectrometry). (3) Results: Ten proteins with significantly different serum concentrations between groups volunteers were: complement-factor-B, apolipoprotein-A-I, fibronectin, alpha-2-HS-glycoprotein, alpha-1B-glycoprotein, heat-shock-cognate-71kDa protein/heat-shock-related-70kDa-protein-2, thymidine phosphorylase-2, cytoplasmic-tryptophan-tRNA-ligase, ficolin-2, beta-Ala-His-dipeptidase. (4) Conclusions: This is the first dynamic LC-MS study performed on a clinical model which differentiates serum proteome of patients in acute phase of ischemic stroke in time series and compares to control group. Listed proteins should be considered as risk factors, markers of ischemic stroke or potential therapeutic targets. Further clinical validation might define their exact role in differential diagnostics, monitoring the course of the ischemic stroke or specifying them as novel drug targets.

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Design and synthesis of novel spirooxindole–indenoquinoxaline derivatives as novel tryptophanyl-tRNA synthetase inhibitors

et al. 2019

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Effect of Mini‐Tyrosyl‐tRNA Synthetase/Mini‐Tryptophanyl‐tRNA Synthetase on Angiogenesis in Rhesus Monkeys after Acute Myocardial Infarction

Cited by 8 publications

References 33 publications

Recessive aminoacyl-tRNA synthetase disorders: lessons learned from in vivo disease models

Recessive aminoacyl-tRNA synthetase disorders: lessons learned from in vivo disease models

New Candidates for Biomarkers and Drug Targets of Ischemic Stroke—A First Dynamic LC-MS Human Serum Proteomic Study

Design and synthesis of novel spirooxindole–indenoquinoxaline derivatives as novel tryptophanyl-tRNA synthetase inhibitors

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