Evidence map›Paper›PMID 34218459›Full record

ArticleHepatology (Baltimore, Md.)2021

The Pannexin 1/Purinergic Receptor P2X4 Pathway Controls the Secretion of MicroRNA-Containing Exosomes by HCV-Infected Hepatocytes.

Ok-Kyung Kim, Da-Eun Nam, Young S Hahn

Open access · greenAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

21 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Altered Pannexin2 Expression in Retinal Degeneration: Insights from the P23H Mouse Model of Retinis Pigmentosa.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
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  8. Review
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  12. Review
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  15. Pannexin1 channels in the liver: an open enemy.Frontiers in cell and developmental biology · 2023
    Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Hepatic pannexin-1 mediates ST2Clinical and translational medicine · 2022
    Article
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

3 authors at 2 institutions in 2 countries.

Ok-Kyung KimBeirne B. Carter Center for Immunology Research, University of Virginia, Charlottesville, VA.
Da-Eun NamBeirne B. Carter Center for Immunology Research, University of Virginia, Charlottesville, VA.ORCID 0000-0002-2765-7323
Young S HahnBeirne B. Carter Center for Immunology Research, University of Virginia, Charlottesville, VA.
Carter Center · USChonnam National University · KR

Funding

Role of HCV exosomes in intercellular communicationR01DK122737 · NIDDK · UNIVERSITY OF VIRGINIA · PI HAHN, YOUNG S. · 2020 to 2024
$2.3M
NIDDK NIH HHS R01 DK122737
6 · The paper itself

Abstract

BACKGROUND AND

aimsHCV infection is a major risk factor that can lead to chronic liver disease, including fibrosis, cirrhosis, and HCC. Progression of chronic liver disease by HCV infection is caused by a complex intercellular reaction. Especially, exosomes and microRNAs (miRNAs) from HCV-infected hepatocytes play a role in the pathogenesis of liver disease by facilitating cellular communication between parenchymal and nonparenchymal cells. However, the underlying mechanism of secretions of exosome and miRNAs during HCV infection is still open for study. APPROACH AND

resultsIn this study, we demonstrated a pathway for the release of exosome and exosomal miRNAs through caspase-3/pannexin 1 (Panx1)/P2X4 activation during HCV infection in hepatocytes. We found that HCV infection induced the stimulation of exosome release and activation of the caspase-3/Panx1/P2X4 pathway in Huh7.5.1 cells. In addition, miR-122 and miR-146a levels in extracellular exosomes from HCV-infected cells were dramatically increased whereas intracellular miR122 and miR-146a expression had no large changes. Notably, secretions of exosomes and exosomal miRNAs were decreased by inhibition of caspase 3, Panx1, and P2X4 whereas inhibition of ROCK-1 cleavage did not affect these during HCV infection in Huh7.5.1 cells.

conclusionsThese results suggested that HCV infection caused secretions of exosomes and exosomal miRNAs dependent on the caspase 3/Panx1/P2X4 pathway. Our study provides a possible therapeutic intervention using Panx1 suppression for liver disease development mediated by exosomes from HCV-infected hepatocytes.

Indexed as

Blotting, WesternCell LineConnexinsExosomesFlow CytometryHepatitis C, ChronicHepatocytesHumansMicroRNAsMicroscopy, FluorescenceNerve Tissue ProteinsReal-Time Polymerase Chain ReactionReceptors, Purinergic P2X4ConnexinsMicroRNAsNerve Tissue ProteinsPANX1 protein, humanReceptors, Purinergic P2X4

Identifiers

PMID34218459
PMCPMC8639610
OpenAlexW3179361148

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.