Evidence map›Paper›PMID 31491992›Full record

ArticleInternational journal of molecular sciences2019

Endoplasmic Reticulum Stress Increases DUSP5 Expression via PERK-CHOP Pathway, Leading to Hepatocyte Death.

Hye Jin Jo, Jin Won Yang, Ji Hye Park, Eul Sig Choi, Chae-Seok Lim, Seoul Lee, Chang Yeob Han

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Role ofbioRxiv : the preprint server for biology · 2023
    Article
  5. The Role ofViruses · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. RIG-I Deficiency Promotes Obesity-Induced Insulin Resistance.Pharmaceuticals (Basel, Switzerland) · 2021
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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 2 institutions in 1 country.

Hye Jin JoDepartment of Pharmacology, School of Medicine, Wonkwang University, Iksan 54538, Jeonbuk, Korea. 546chj@naver.com.
Jin Won YangCollege of Pharmacy, Woosuk University, Wanju 55338, Jeonbuk, Korea. jwyang@woosuk.ac.kr.
Ji Hye ParkDepartment of Pharmacology, School of Medicine, Wonkwang University, Iksan 54538, Jeonbuk, Korea. ks7384@gmail.com.
Eul Sig ChoiDepartment of Pharmacology, School of Medicine, Wonkwang University, Iksan 54538, Jeonbuk, Korea. eschoie@hanmail.net.
Chae-Seok LimDepartment of Pharmacology, School of Medicine, Wonkwang University, Iksan 54538, Jeonbuk, Korea. cslimwk1@wku.ac.kr.
Seoul LeeDepartment of Pharmacology, School of Medicine, Wonkwang University, Iksan 54538, Jeonbuk, Korea. stress@wku.ac.kr.
Chang Yeob HanDepartment of Pharmacology, School of Medicine, Wonkwang University, Iksan 54538, Jeonbuk, Korea. hancy17@wku.ac.kr.
Wonkwang University · KRWoosuk University · KR

Funding

Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education 2017R1D1A1B03028272
6 · The paper itself

Abstract

Hepatocyte death is critical for the pathogenesis of liver disease progression, which is closely associated with endoplasmic reticulum (ER) stress responses. However, the molecular basis for ER stress-mediated hepatocyte injury remains largely unknown. This study investigated the effect of ER stress on dual-specificity phosphatase 5 (DUSP5) expression and its role in hepatocyte death. Analysis of Gene Expression Omnibus (GEO) database showed that hepatic DUSP5 levels increased in the patients with liver fibrosis, which was verified in mouse models of liver diseases with ER stress. DUSP5 expression was elevated in both fibrotic and acutely injured liver of mice treated with liver toxicants. Treatment of ER stress inducers enhanced DUSP5 expression in hepatocytes, which was validated in vivo condition. The induction of DUSP5 by ER stress was blocked by either treatment with a chemical inhibitor of the protein kinase RNA-like endoplasmic reticulum kinase (PERK) pathway, or knockdown of C/EBP homologous protein (CHOP), whereas it was not affected by the silencing of IRE1 or ATF6. In addition, DUSP5 overexpression decreased extracellular-signal-regulated kinase (ERK) phosphorylation, but increased cleaved caspase-3 levels. Moreover, the reduction of cell viability under ER stress condition was attenuated by DUSP5 knockdown. In conclusion, DUSP5 expression is elevated in hepatocytes by ER stress through the PERK-CHOP pathway, contributing to hepatocyte death possibly through ERK inhibition.

Indexed as

Endoplasmic Reticulum StressSignal TransductionAnimalsApoptosisCell DeathDual-Specificity PhosphataseseIF-2 KinaseGene ExpressionHepatocytesHumansLiver DiseasesMiceTranscription Factor CHOPDDIT3 protein, humanDual-Specificity PhosphatasesDUSP5 protein, humanEIF2AK3 protein, humaneIF-2 KinaseTranscription Factor CHOPcell deathCHOPDUSP5ER stresshepatocytePERK

Identifiers

PMID31491992
PMCPMC6770509
OpenAlexW2972106604

What OpenQuestion holds

Textmetadata
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.