Evidence map›Paper›PMID 29029277›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2018

miR-122 Release in Exosomes Precedes Overt Tolvaptan-Induced Necrosis in a Primary Human Hepatocyte Micropatterned Coculture Model.

Merrie Mosedale, J Scott Eaddy, O Joseph Trask, Natalie S Holman, Kristina K Wolf, Edward LeCluyse, Brenton R Ware, Salman R Khetani, Jingtao Lu, William J Brock and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.7field-weighted citation impact, top 5% 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

22 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
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  9. Characterization of primary mouse hepatocyte spheroids as a model system to support investigations of drug-induced liver injury.Toxicology in vitro : an international journal published in association with BIBRA · 2021
    Article
  10. Article
  11. Frontiers in immunology · 2021
    Review
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  16. Identification of Candidate Risk Factor Genes for Human Idelalisib Toxicity Using a Collaborative Cross Approach.Toxicological sciences : an official journal of the Society of Toxicology · 2019
    Article
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  18. Article
  19. Review
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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

12 authors at 3 institutions in 1 country.

Merrie MosedaleInstitute for Drug Safety Sciences, University of North Carolina at Chapel Hill, Research Triangle Park, North Carolina 27709.
J Scott EaddyInstitute for Drug Safety Sciences, University of North Carolina at Chapel Hill, Research Triangle Park, North Carolina 27709.
O Joseph TraskInstitute for Drug Safety Sciences, University of North Carolina at Chapel Hill, Research Triangle Park, North Carolina 27709.
Natalie S HolmanInstitute for Drug Safety Sciences, University of North Carolina at Chapel Hill, Research Triangle Park, North Carolina 27709.
Kristina K WolfInstitute for Drug Safety Sciences, University of North Carolina at Chapel Hill, Research Triangle Park, North Carolina 27709.
Edward LeCluyseInstitute for Drug Safety Sciences, University of North Carolina at Chapel Hill, Research Triangle Park, North Carolina 27709.
Brenton R WareSchool of Biomedical Engineering, Colorado State University, Fort Collins, Colorado 80523.
Salman R KhetaniDepartment of Bioengineering, University of Illinois at Chicago, Chicago, Illinois 60607.
Jingtao LuInstitute for Drug Safety Sciences, University of North Carolina at Chapel Hill, Research Triangle Park, North Carolina 27709.
William J BrockOtsuka Pharmaceutical Development & Commercialization, Inc, Rockville, Maryland 20850.
Sharin E RothOtsuka Pharmaceutical Development & Commercialization, Inc, Rockville, Maryland 20850.
Paul B WatkinsInstitute for Drug Safety Sciences, University of North Carolina at Chapel Hill, Research Triangle Park, North Carolina 27709.
University of North Carolina at Chapel Hill · USPharmaceutical Product Development (United States) · USUniversity of Illinois Chicago · US

Funding

TOXICOLOGYT32ES007126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ILONA JASPERS, Bernard E. Weissman · 1985 to 2026
$13.0M
NIEHS NIH HHS T32 ES007126
6 · The paper itself

Abstract

Idiosyncratic drug-induced liver injury (IDILI) is thought to often result from an adaptive immune attack on the liver. However, it has been proposed that the cascade of events culminating in an adaptive immune response begins with drug-induced hepatocyte stress, release of exosomal danger signals, and innate immune activation, all of which may occur in the absence of significant hepatocelluar death. A micropatterned coculture model (HepatoPac) was used to explore the possibility that changes in exosome content precede overt necrosis in response to the IDILI drug tolvaptan. Hepatocytes from 3 human donors were exposed to a range of tolvaptan concentrations bracketing plasma Cmax or DMSO control continuously for 4, 24, or 72 h. Although alanine aminotransferase release was not significantly affected at any concentration, tolvaptan exposures at approximately 30-fold median plasma Cmax resulted in increased release of exosomal microRNA-122 (miR-122) into the medium. Cellular imaging and microarray analysis revealed that the most significant increases in exosomal miR-122 were associated with programmed cell death and small increases in membrane permeability. However, early increases in exosome miR-122 were more associated with mitochondrial-induced apoptosis and oxidative stress. Taken together, these data suggest that tolvaptan treatment induces cellular stress and exosome release of miR-122 in primary human hepatocytes in the absence of overt necrosis, providing direct demonstration of this with a drug capable of causing IDILI. In susceptible individuals, these early events may occur at pharmacologic concentrations of tolvaptan and may promote an adaptive immune attack that ultimately results in clinically significant liver injury.

Indexed as

Adaptive ImmunityAdultApoptosisCells, CulturedCell SurvivalCoculture TechniquesExosomesFemaleHepatocytesHumansImmunity, InnateMaleMembrane Potential, MitochondrialMicroRNAsMiddle AgedOxidative StressMicroRNAsMIRN122 microRNA, humanTolvaptanapoptosisdanger signalidiosyncratic drug-induced liver injury (IDILI)mitochondrial dysfunctionoxidative stress

Identifiers

PMID29029277
PMCPMC6257010
OpenAlexW2759627007

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.