Cellular signaling crosstalk between Wnt signaling and gap junctions inbenzo[a]pyrene toxicity
DC Field | Value | Language |
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dc.contributor.author | Won, Dong-Hoon | - |
dc.contributor.author | Hwang, Da-Bin | - |
dc.contributor.author | Shin, Yoo-Sub | - |
dc.contributor.author | Kim, Shin-Young | - |
dc.contributor.author | Kim, Changuk | - |
dc.contributor.author | Hong, In-Sun | - |
dc.contributor.author | Kang, Byeong-Cheol | - |
dc.contributor.author | Che, Jeong-Hwan | - |
dc.contributor.author | Yun, Jun-Won | - |
dc.date.accessioned | 2023-04-14T02:40:08Z | - |
dc.date.available | 2023-04-14T02:40:08Z | - |
dc.date.created | 2021-07-28 | - |
dc.date.issued | 2023-02 | - |
dc.identifier.issn | 0742-2091 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/87465 | - |
dc.description.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/beta-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/beta-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/beta-catenin signaling related to the PI3K-Akt pathway. To identify the relationship between GJIC and Wnt/beta-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/beta-catenin signaling negatively regulates GJIC. Despite the inverse correlation between Wnt/beta-catenin signaling and Cx43 promoter activation as indicated by downregulation of beta-catenin nuclear translocation and upregulation of Cx43 promoter activation involving HNF3 beta, 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/beta-catenin signaling. More importantly, linking Wnt/beta-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. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | SPRINGER | - |
dc.relation.isPartOf | CELL BIOLOGY AND TOXICOLOGY | - |
dc.title | Cellular signaling crosstalk between Wnt signaling and gap junctions inbenzo[a]pyrene toxicity | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000675092100002 | - |
dc.identifier.doi | 10.1007/s10565-021-09630-z | - |
dc.identifier.bibliographicCitation | CELL BIOLOGY AND TOXICOLOGY, v.39, no.1, pp.165 - 182 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.scopusid | 2-s2.0-85110893594 | - |
dc.citation.endPage | 182 | - |
dc.citation.startPage | 165 | - |
dc.citation.title | CELL BIOLOGY AND TOXICOLOGY | - |
dc.citation.volume | 39 | - |
dc.citation.number | 1 | - |
dc.contributor.affiliatedAuthor | Hong, In-Sun | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | Benzo[a]pyrene | - |
dc.subject.keywordAuthor | Gap junction | - |
dc.subject.keywordAuthor | Connexin 43 | - |
dc.subject.keywordAuthor | Wnt | - |
dc.subject.keywordAuthor | beta-catenin | - |
dc.subject.keywordAuthor | Toxicity | - |
dc.subject.keywordPlus | BETA-CATENIN | - |
dc.subject.keywordPlus | RAT-LIVER | - |
dc.subject.keywordPlus | INTERCELLULAR COMMUNICATION | - |
dc.subject.keywordPlus | TUMOR-SUPPRESSOR | - |
dc.subject.keywordPlus | DNA-DAMAGE | - |
dc.subject.keywordPlus | CELLS | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | PATHWAY | - |
dc.subject.keywordPlus | CANCER | - |
dc.subject.keywordPlus | HEPATOCARCINOGENESIS | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalResearchArea | Toxicology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Toxicology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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