Evidence map›Paper›PMID 35483669›Full record

ArticleToxicology and applied pharmacology2022

Combining phenotypic profiling and targeted RNA-Seq reveals linkages between transcriptional perturbations and chemical effects on cell morphology: Retinoic acid as an example.

Johanna Nyffeler, Clinton Willis, Felix R Harris, Laura W Taylor, Richard Judson, Logan J Everett, Joshua A Harrill

Open access · greenAbstract read
In one paragraph

Article in Toxicology and applied pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.2field-weighted citation impact, top 12% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 26 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Johanna NyffelerCenter for Computational Toxicology & Exposure, Office of Research and Development, US Environmental Protection Agency, Durham, NC 27711, United States of America; Oak Ridge Institute for Science and Education (ORISE) Postdoctoral Fellow, Oak Ridge, TN 37831, United States of America.
Clinton WillisCenter for Computational Toxicology & Exposure, Office of Research and Development, US Environmental Protection Agency, Durham, NC 27711, United States of America.
Felix R HarrisCenter for Computational Toxicology & Exposure, Office of Research and Development, US Environmental Protection Agency, Durham, NC 27711, United States of America; Oak Ridge Associated Universities (ORAU) National Student Services Contractor, Oak Ridge, TN 37831, United States of America.
Laura W TaylorCenter for Computational Toxicology & Exposure, Office of Research and Development, US Environmental Protection Agency, Durham, NC 27711, United States of America.
Richard JudsonCenter for Computational Toxicology & Exposure, Office of Research and Development, US Environmental Protection Agency, Durham, NC 27711, United States of America.
Logan J EverettCenter for Computational Toxicology & Exposure, Office of Research and Development, US Environmental Protection Agency, Durham, NC 27711, United States of America.
Joshua A HarrillCenter for Computational Toxicology & Exposure, Office of Research and Development, US Environmental Protection Agency, Durham, NC 27711, United States of America. Electronic address: harrill.joshua@epa.gov.
Environmental Protection Agency · USOak Ridge Associated Universities · US

Funding

Intramural EPA EPA999999
6 · The paper itself

Abstract

The United States Environmental Protection Agency has proposed a tiered testing strategy for chemical hazard evaluation based on new approach methods (NAMs). The first tier includes in vitro profiling assays applicable to many (human) cell types, such as high-throughput transcriptomics (HTTr) and high-throughput phenotypic profiling (HTPP). The goals of this study were to: (1) harmonize the seeding density of U-2 OS human osteosarcoma cells for use in both assays; (2) compare HTTr- versus HTPP-derived potency estimates for 11 mechanistically diverse chemicals; (3) identify candidate reference chemicals for monitoring assay performance in future screens; and (4) characterize the transcriptional and phenotypic changes in detail for all-trans retinoic acid (ATRA) as a model compound known for its adverse effects on osteoblast differentiation. The results of this evaluation showed that (1) HTPP conducted at low (400 cells/well) and high (3000 cells/well) seeding densities yielded comparable potency estimates and similar phenotypic profiles for the tested chemicals; (2) HTPP and HTTr resulted in comparable potency estimates for changes in cellular morphology and gene expression, respectively; (3) three test chemicals (etoposide, ATRA, dexamethasone) produced concentration-dependent effects on cellular morphology and gene expression that were consistent with known modes-of-action, demonstrating their suitability for use as reference chemicals for monitoring assay performance; and (4) ATRA produced phenotypic changes that were highly similar to other retinoic acid receptor activators (AM580, arotinoid acid) and some retinoid X receptor activators (bexarotene, methoprene acid). This phenotype was observed concurrently with autoregulation of the RARB gene. Both effects were prevented by pre-treating U-2 OS cells with pharmacological antagonists of their respective receptors. Thus, the observed phenotype could be considered characteristic of retinoic acid pathway activation in U-2 OS cells. These findings lay the groundwork for combinatorial screening of chemicals using HTTr and HTPP to generate complementary information for the first tier of a NAM-based chemical hazard evaluation strategy.

Indexed as

Bone NeoplasmsTretinoinHumansPhenotypeReceptors, Retinoic AcidRNA-SeqUnited StatesReceptors, Retinoic AcidTretinoinCell PaintingComputational ToxicologyConcentration-ResponseHigh-Throughput Phenotypic Profiling

Identifiers

PMID35483669
PMCPMC10894461
OpenAlexW4224881220

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.