Evidence map›Paper›PMID 37815672›Full record

ArticleEuropean journal of drug metabolism and pharmacokinetics2023

The Effects of 16-HETE Enantiomers on Hypertrophic Markers in Human Fetal Ventricular Cardiomyocytes, RL-14 Cells.

Rahmat Hidayat, Mahmoud A El-Ghiaty, Sherif M Shoieb, Mohammed A Alqahtani, Ayman O S El-Kadi

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Article in European journal of drug metabolism and pharmacokinetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

3 citing papers in PubMed, 5 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

5 authors at 1 institution in 1 country.

Rahmat HidayatFaculty of Pharmacy and Pharmaceutical Sciences, 2142J Katz Group-Rexall Centre for Pharmacy and Health Research, University of Alberta, Edmonton, Alberta, T6G 2E1, Canada.
Mahmoud A El-GhiatyFaculty of Pharmacy and Pharmaceutical Sciences, 2142J Katz Group-Rexall Centre for Pharmacy and Health Research, University of Alberta, Edmonton, Alberta, T6G 2E1, Canada.
Sherif M ShoiebFaculty of Pharmacy and Pharmaceutical Sciences, 2142J Katz Group-Rexall Centre for Pharmacy and Health Research, University of Alberta, Edmonton, Alberta, T6G 2E1, Canada.
Mohammed A AlqahtaniFaculty of Pharmacy and Pharmaceutical Sciences, 2142J Katz Group-Rexall Centre for Pharmacy and Health Research, University of Alberta, Edmonton, Alberta, T6G 2E1, Canada.
Ayman O S El-KadiFaculty of Pharmacy and Pharmaceutical Sciences, 2142J Katz Group-Rexall Centre for Pharmacy and Health Research, University of Alberta, Edmonton, Alberta, T6G 2E1, Canada. aelkadi@ualberta.ca.ORCID http://orcid.org/0000-0002-8692-0400
University of Alberta · CA

Funding

CIHR CIHR PS 168846
6 · The paper itself

Abstract

backgroundCytochrome P450 (CYP) metabolizes arachidonic acid to produce bioactive metabolites such as EETs and HETEs: mid-chain, subterminal, and terminal HETEs. Recent studies have revealed the role of CYP1B1 and its associated cardiotoxic mid-chain HETE metabolites in developing cardiac hypertrophy and heart failure. Subterminal HETEs have also been involved in various physiological and pathophysiological processes; however, their role in cardiac hypertrophy has not been fully defined.

objectiveThe objective of the current study is to determine the possible effect of subterminal HETEs, R and S enantiomers of 16-HETE, on CYP1B1 expression in vitro using human cardiomyocytes RL-14 cells.

methodsIn the study, RL14 cell line was treated with vehicle and either of the 16-HETE enantiomers for 24 h. Subsequently, the following markers were assessed: cell viability, cellular size, hypertrophic markers, CYP1B1 gene expression (at mRNA, protein, and activity levels), luciferase activity, and CYP1B1 mRNA and protein half-lives.

resultsThe results of the study showed that 16-HETE enantiomers significantly increased hypertrophic markers and upregulated CYP1B1 mRNA and protein expressions in RL-14 cell line. The upregulation of CYP1B1 by 16-HETE enantiomers occurs via a transcriptional mechanism as evidenced by transcriptional induction and luciferase reporter assay. Furthermore, neither post-transcriptional nor post-translational modification was involved in such modulation since there was no change in CYP1B1 mRNA and protein stabilities upon treatment with 16-HETE enantiomers.

conclusionThe current study provides the first evidence that 16R-HETE and 16S-HETE increase CYP1B1 gene expression through a transcriptional mechanism.

Indexed as

Hydroxyeicosatetraenoic AcidsMyocytes, CardiacCardiomegalyHumansLuciferasesRNA, Messenger16-hydroxy-5,8,11,14-eicosatetraenoic acidHydroxyeicosatetraenoic AcidsLuciferasesRNA, Messenger

Identifiers

PMID37815672
OpenAlexW4387472477

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.