Evidence map›Paper›PMID 28077652›Full record

ArticleJournal of virology2017

Exosome-Mediated Intercellular Communication between Hepatitis C Virus-Infected Hepatocytes and Hepatic Stellate Cells.

Pradip B Devhare, Reina Sasaki, Shubham Shrivastava, Adrian M Di Bisceglie, Ranjit Ray, Ratna B Ray

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 137 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed, 1 pooled it
8.6field-weighted citation impact, top 2% 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

137 citing papers in PubMed, 1 synthesis or guideline pooled it, 184 citations in OpenAlex.

  1. Pooled it
  2. Review
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  6. Review
  7. Epigenetic Mechanisms Involved in Hcv Infection and Human HCC.International journal of molecular sciences · 2025
    Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Sinusoidal communication in chronic liver disease.Clinical and molecular hepatology · 2025
    Review
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  17. Review
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  19. Review
  20. Article

77 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Pradip B DevhareDepartment of Pathology, Saint Louis University, Saint Louis, Missouri, USA.
Reina SasakiDepartment of Pathology, Saint Louis University, Saint Louis, Missouri, USA.
Shubham ShrivastavaDepartment of Pathology, Saint Louis University, Saint Louis, Missouri, USA.
Adrian M Di BisceglieDepartment of Internal Medicine, Saint Louis University, Saint Louis, Missouri, USA.
Ranjit RayDepartment of Internal Medicine, Saint Louis University, Saint Louis, Missouri, USA.
Ratna B RayDepartment of Pathology, Saint Louis University, Saint Louis, Missouri, USA rayrb@slu.edu.
Saint Louis University · US

Funding

Innate Immunity and Hepatitis C Virus InfectionR01DK081817 · NIDDK · SAINT LOUIS UNIVERSITY · PI RAY, RATNA B. · 2009 to 2020
$3.3M
NIDDK NIH HHS R01 DK081817
6 · The paper itself

Abstract

Fibrogenic pathways in the liver are principally regulated by activation of hepatic stellate cells (HSC). Fibrosis is associated with chronic hepatitis C virus (HCV) infection, although the mechanism is poorly understood. HSC comprise the major population of nonparenchymal cells in the liver. Since HCV does not replicate in HSC, we hypothesized that exosomes secreted from HCV-infected hepatocytes activate HSC. Primary or immortalized human hepatic stellate (LX2) cells were exposed to exosomes derived from HCV-infected hepatocytes (HCV-exo), and the expression of fibrosis-related genes was examined. Our results demonstrated that HCV-exo internalized to HSC and increased the expression of profibrotic markers. Further analysis suggested that HCV-exo carry miR-19a and target SOCS3 in HSC, which in turn activates the STAT3-mediated transforming growth factor β (TGF-β) signaling pathway and enhances fibrosis marker genes. The higher expression of miR-19a in exosomes was also observed from HCV-infected hepatocytes and in sera of chronic HCV patients with fibrosis compared to healthy volunteers and non-HCV-related liver disease patients with fibrosis. Together, our results demonstrated that miR-19a carried through the exosomes from HCV-infected hepatocytes activates HSC by modulating the SOCS-STAT3 axis. Our results implicated a novel mechanism of exosome-mediated intercellular communication in the activation of HSC for liver fibrosis in HCV infection.

Indexed as

Cell CommunicationCells, CulturedEndocytosisExosomesGene Expression ProfilingGene Expression RegulationHepatic Stellate CellsHepatitis C, ChronicHepatocytesHumansMicroRNAsSignal TransductionSuppressor of Cytokine Signaling 3 ProteinMicroRNAsMIRN19A microRNA, humanSOCS3 protein, humanSuppressor of Cytokine Signaling 3 Proteinexosomeshepatic stellate cellshepatitis C virusliver fibrosismicroRNAmiRNAs

Identifiers

PMID28077652
PMCPMC5331806
OpenAlexW2575061790

What OpenQuestion 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 OpenQuestion graph.