ArticleInternational journal of molecular sciences2015
Elucidating mechanisms of toxicity using phenotypic data from primary human cell systems--a chemical biology approach for thrombosis-related side effects.
Article in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Exploring In Vivo Models of Musculoskeletal Frailty: A Comprehensive Systematic Review.International journal of molecular sciences · 2023Pooled it
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- Use of a rapid human primary cell-based disease screening model, to compare next generation products to combustible cigarettes.Current research in toxicology · 2021Article
- The activities of drug inactive ingredients on biological targets.Science (New York, N.Y.) · 2020Article
- Assessing bioactivity-exposure profiles of fruit and vegetable extracts in the BioMAP profiling system.Toxicology in vitro : an international journal published in association with BIBRA · 2019Article
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- The Role of Autophagy in Chondrocyte Metabolism and Osteoarthritis: A Comprehensive Research Review.BioMed research international · 2019Review
- Human Cell-BasedFrontiers in big data · 2019Article
- Identification of potential aryl hydrocarbon receptor ligands by virtual screening of industrial chemicals.Environmental science and pollution research international · 2018Article
- Role of autophagy in cell-penetrating peptide transfection model.Scientific reports · 2017Article
- Screening for angiogenic inhibitors in zebrafish to evaluate a predictive model for developmental vascular toxicity.Reproductive toxicology (Elmsford, N.Y.) · 2017Article
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Here we describe a chemical biology approach for elucidating potential toxicity mechanisms for thrombosis-related side effects. This work takes advantage of a large chemical biology data set comprising the effects of known, well-characterized reference agents on the cell surface levels of tissue factor (TF) in a primary human endothelial cell-based model of vascular inflammation, the BioMAP® 3C system. In previous work with the Environmental Protection Agency (EPA) for the ToxCast™ program, aryl hydrocarbon receptor (AhR) agonists and estrogen receptor (ER) antagonists were found to share an usual activity, that of increasing TF levels in this system. Since human exposure to compounds in both chemical classes is associated with increased incidence of thrombosis-related side effects, we expanded this analysis with a large number of well-characterized reference compounds in order to better understand the underlying mechanisms. As a result, mechanisms for increasing (AhR, histamine H1 receptor, histone deacetylase or HDAC, hsp90, nuclear factor kappa B or NFκB, MEK, oncostatin M receptor, Jak kinase, and p38 MAPK) and decreasing (vacuolar ATPase or V-ATPase) and mTOR) TF expression levels were uncovered. These data identify the nutrient, lipid, bacterial, and hypoxia sensing functions of autophagy as potential key regulatory points controlling cell surface TF levels in endothelial cells and support the mechanistic hypothesis that these functions are associated with thrombosis-related side effects in vivo.
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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.