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Proliferation of prostate epithelia induced by IL-6 from stroma reacted with Trichomonasvaginalis

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dc.contributor.authorKim, J. -H.-
dc.contributor.authorHan, I. -H.-
dc.contributor.authorKim, Y. -S.-
dc.contributor.authorNoh, C. -S.-
dc.contributor.authorRyu, J. -S.-
dc.date.accessioned2022-07-11T17:20:35Z-
dc.date.available2022-07-11T17:20:35Z-
dc.date.created2021-05-12-
dc.date.issued2018-06-
dc.identifier.issn0141-9838-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/149920-
dc.description.abstractBenign prostatic hyperplasia (BPH) is characterized by the proliferation of stromal and epithelial cell types in the prostate, and interactions between the two types of cells. We demonstrated previously that proliferation of prostate stromal cells was induced by BPH epithelial cells in response to Trichomonasvaginalis (Tv) infection via crosstalk with mast cells. In this study, we investigated whether IL-6 released by the proliferating stromal cells in turn induce the BPH epithelial cells to multiply. When culture supernatants of the proliferating prostate stromal cells were added to BPH epithelial cells, the latter multiplied, and expression of cyclin D1, FGF2 and Bcl-2 increased. Blocking the IL-6 signalling pathway with anti-IL-6R antibody or JAK1/2 inhibitor inhibited the proliferation of the BPH epithelial cells and reduced the expression of IL-6, IL-6R and STAT3. Also, epithelial-mesenchymal transition was detected in the proliferating BPH epithelial cells. In conclusion, IL-6 released from proliferating prostate stromal cells induced by BPH epithelial cells infected with Tv in turn induces multiplication of the BPH epithelial cells. This result provides first evidence that the inflammatory microenvironment of prostate stromal cells resulting from Tv infection induces the proliferation of prostate epithelial cells by stromal-epithelial interaction.-
dc.language영어-
dc.language.isoen-
dc.publisherWILEY-
dc.titleProliferation of prostate epithelia induced by IL-6 from stroma reacted with Trichomonasvaginalis-
dc.typeArticle-
dc.contributor.affiliatedAuthorKim, Y. -S.-
dc.contributor.affiliatedAuthorRyu, J. -S.-
dc.identifier.doi10.1111/pim.12531-
dc.identifier.scopusid2-s2.0-85048032880-
dc.identifier.wosid000434155500003-
dc.identifier.bibliographicCitationPARASITE IMMUNOLOGY, v.40, no.6, pp.1 - 9-
dc.relation.isPartOfPARASITE IMMUNOLOGY-
dc.citation.titlePARASITE IMMUNOLOGY-
dc.citation.volume40-
dc.citation.number6-
dc.citation.startPage1-
dc.citation.endPage9-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaImmunology-
dc.relation.journalResearchAreaParasitology-
dc.relation.journalWebOfScienceCategoryImmunology-
dc.relation.journalWebOfScienceCategoryParasitology-
dc.subject.keywordPlusMESENCHYMAL TRANSITION-
dc.subject.keywordPlusINFLAMMATORY RESPONSES-
dc.subject.keywordPlusSIGNALING PATHWAY-
dc.subject.keywordPlusBENIGN-
dc.subject.keywordPlusHYPERPLASIA-
dc.subject.keywordPlusVAGINALIS-
dc.subject.keywordPlusCANCER-
dc.subject.keywordPlusCELLS-
dc.subject.keywordPlusINTERLEUKIN-6-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordAuthorcytokines-
dc.subject.keywordAuthorinflammation-
dc.subject.keywordAuthorprostatic hyperplasia-
dc.subject.keywordAuthorprotozoan infections-
dc.identifier.urlhttps://onlinelibrary.wiley.com/doi/10.1111/pim.12531-
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서울 의과대학 > 서울 환경의생물학교실 > 1. Journal Articles
서울 의과대학 > 서울 생화학·분자생물학교실 > 1. Journal Articles

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COLLEGE OF MEDICINE (DEPARTMENT OF BIOCHEMISTRY & MOLECULAR BIOLOGY)
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