Evidence map›Paper›PMID 34283317›Full record

ArticleCell biology and toxicology2023

Cellular signaling crosstalk between Wnt signaling and gap junctions inbenzo[a]pyrene toxicity.

Dong-Hoon Won, Da-Bin Hwang, Yoo-Sub Shin, Shin-Young Kim, Changuk Kim, In-Sun Hong, Byeong-Cheol Kang, Jeong-Hwan Che, Jun-Won Yun

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Article in Cell biology and toxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 41% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
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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

9 authors at 4 institutions in 3 countries.

Dong-Hoon WonDepartment of Biotechnology, The Catholic University of Korea, Bucheon, 14662, South Korea.
Da-Bin HwangDepartment of Biotechnology, The Catholic University of Korea, Bucheon, 14662, South Korea.
Yoo-Sub ShinDepartment of Biotechnology, The Catholic University of Korea, Bucheon, 14662, South Korea.
Shin-Young KimDepartment of Biotechnology, The Catholic University of Korea, Bucheon, 14662, South Korea.
Changuk KimDepartment of Biotechnology, The Catholic University of Korea, Bucheon, 14662, South Korea.
In-Sun HongDepartment of Molecular Medicine, School of Medicine, Gachon University, Incheon, 21999, South Korea.
Byeong-Cheol KangGraduate School of Translational Medicine, Seoul National University College of Medicine, Seoul, 03080, South Korea.
Jeong-Hwan CheBiomedical Center for Animal Resource and Development, Seoul National University College of Medicine, Seoul, 03080, South Korea. casache@snu.ac.kr.
Jun-Won YunDepartment of Biotechnology, The Catholic University of Korea, Bucheon, 14662, South Korea. jwyun@catholic.ac.kr.ORCID 0000-0002-0155-4190
The Catholic University of Korea Bucheon St. Mary's Hospital · KRSeoul National University · KRCatholic Medical Center · USGachon University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gap junctional intercellular communication (GJIC) is considered a key biological mechanism to maintain homeostasis in cell differentiation and growth. In addition, as another major signaling pathway associated with cell proliferation and differentiation, Wnt/β-catenin signaling appears to trigger several cellular responses against injury. The purpose of the present study was to investigate the effects of a known toxic agent, benzo[a]pyrene (BaP), on the regulation and interaction between GJIC and Wnt/β-catenin signaling. BaP treatment resulted in GJIC inhibition and decreases the major GJIC protein connexin 43 (Cx43) in WB-F344 rat liver epithelial cells. We also found BaP-mediated downregulation of Wnt/β-catenin signaling related to the PI3K-Akt pathway. To identify the relationship between GJIC and Wnt/β-catenin signaling, we treated WB-F344 cells with the Wnt agonist CHIR99021 and found that it inhibited GJIC while causing a significant reduction in Cx43 expression at both the mRNA and protein levels, through the repression of promoter activity. This Wnt agonist-mediated GJIC inhibition was confirmed using a small interfering RNA directed against the Wnt antagonist Dact2, indicating that Wnt/β-catenin signaling negatively regulates GJIC. Despite the inverse correlation between Wnt/β-catenin signaling and Cx43 promoter activation as indicated by downregulation of β-catenin nuclear translocation and upregulation of Cx43 promoter activation involving HNF3β, BaP treatment decreased the Cx43 protein expression, which was associated with protein degradation, possibly through protein kinase C activation. In conclusion, our results revealed the mechanism of BaP-induced inhibition of GJIC and Wnt/β-catenin signaling. More importantly, linking Wnt/β-catenin signaling to Cx protein expression will have profound implications in understanding the relationships among different major signaling pathways associated with cell proliferation and differentiation in toxicity.

Indexed as

beta CateninConnexin 43AnimalsGap JunctionsNuclear ProteinsPhosphatidylinositol 3-KinasesPyrenesRatsRats, Inbred F344Wnt Signaling Pathwaybeta CateninConnexin 43Dact2 protein, ratNuclear ProteinsPhosphatidylinositol 3-KinasesPyrenesBenzo[a]pyreneConnexin 43Gap junctionToxicityWntβ-catenin

Identifiers

PMID34283317
OpenAlexW3185400173

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.