Evidence map›Paper›PMID 26121241›Full record

ArticlePloS one2015

Substitution in Amino Acid 70 of Hepatitis C Virus Core Protein Changes the Adipokine Profile via Toll-Like Receptor 2/4 Signaling.

Satoko Uraki, Masahiko Tameda, Kazushi Sugimoto, Katsuya Shiraki, Yoshiyuki Takei, Tsutomu Nobori, Masaaki Ito

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. [Hepatitis B core antigen promotes invasion of hepatocellular carcinoma cell line HepG2.2.15 via Toll-like receptor 4].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2017
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. 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

7 authors at 1 institution in 1 country.

Satoko UrakiFirst Department of Internal Medicine, Mie University School of Medicine, Tsu, Japan.
Masahiko TamedaFirst Department of Internal Medicine, Mie University School of Medicine, Tsu, Japan; Department of Molecular and Laboratory Medicine, Mie University School of Medicine, 2-174 Edobashi, Tsu, Mie, 514-8507, Japan; Department of Gastroenterology and Hepatology, Mie University School of Medicine, Tsu, Japan.
Kazushi SugimotoFirst Department of Internal Medicine, Mie University School of Medicine, Tsu, Japan; Department of Molecular and Laboratory Medicine, Mie University School of Medicine, 2-174 Edobashi, Tsu, Mie, 514-8507, Japan; Department of Gastroenterology and Hepatology, Mie University School of Medicine, Tsu, Japan.
Katsuya ShirakiFirst Department of Internal Medicine, Mie University School of Medicine, Tsu, Japan; Department of Gastroenterology and Hepatology, Mie University School of Medicine, Tsu, Japan.
Yoshiyuki TakeiDepartment of Gastroenterology and Hepatology, Mie University School of Medicine, Tsu, Japan.
Tsutomu NoboriDepartment of Molecular and Laboratory Medicine, Mie University School of Medicine, 2-174 Edobashi, Tsu, Mie, 514-8507, Japan.
Masaaki ItoFirst Department of Internal Medicine, Mie University School of Medicine, Tsu, Japan.
Mie University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsIt has been suggested that amino acid (aa) substitution at position 70 from arginine (70R) to glutamine (70Q) in the genotype 1b hepatitis C virus (HCV) core protein is associated with insulin resistance and worse prognosis. However, the precise mechanism is still unclear. The aim of this study was to investigate the impact of the substitution at position 70 in HCV core protein on adipokine production by murine and human adipocytes.

methodsThe influence of treatment with HCV core protein (70R or 70Q) on adipokine production by both 3T3-L1 and human adipocytes were examined with real-time PCR and enzyme-linked immunosorbent assay (ELISA), and triglyceride content was also analyzed. The effects of toll-like receptor (TLR)2/4 inhibition on IL-6 production by 3T3-L1 induced by HCV core protein were examined.

resultsIL-6 production was significantly increased and adiponectin production was reduced without a change in triglyceride content by treatment with 70Q compared to 70R core protein in both murine and human adipocytes. IL-6 induction of 3T3-L1 cells treated by 70Q HCV core protein was significantly inhibited with anti-TLR2 antibody by 42%, and by TLR4 inhibitor by 40%.

conclusionsOur study suggests that extracellular HCV core protein with substitution at position 70 enhanced IL-6 production and reduced adiponectin production from visceral adipose tissue, which can cause insulin resistance, hepatic steatosis, and ultimately development of HCC.

Indexed as

Amino Acid SubstitutionSignal Transduction3T3-L1 CellsAdipocytesAdipokinesAnimalsHumansInterleukin-6MiceRNA, MessengerToll-Like Receptor 2Toll-Like Receptor 4TriglyceridesViral Core ProteinsAdipokinesInterleukin-6nucleocapsid protein, Hepatitis C virusRNA, MessengerToll-Like Receptor 2Toll-Like Receptor 4TriglyceridesViral Core Proteins

Identifiers

PMID26121241
PMCPMC4487891
OpenAlexW1589407406

What OpenQuestion holds

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LicenceCC BY
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.