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The effects of platelet-rich plasma on hypertrophic scars fibroblasts

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dc.contributor.authorNam, Seung Min-
dc.contributor.authorKim, Yong Bae-
dc.date.accessioned2021-08-11T11:44:14Z-
dc.date.available2021-08-11T11:44:14Z-
dc.date.issued2018-08-
dc.identifier.issn1742-4801-
dc.identifier.issn1742-481X-
dc.identifier.urihttps://scholarworks.bwise.kr/sch/handle/2021.sw.sch/5786-
dc.description.abstractWe hypothesised that a feedback mechanism of the transforming growth factor (TGF)-beta 1 signalling pathway, triggered by high-level TGF-beta 1, activates platelet-rich plasma (PRP) release to reduce connective tissue growth factor (CTGF) production and expression of CTGF mRNA in hypertrophic scar dermal fibroblasts. Primary dermal fibroblasts were isolated from cultures of hypertrophic scars. Cells were cultured after addition of serum-free Dulbecco's modified Eagle's medium supplemented with 5% (wt/vol) PRP or platelet-poor plasma (PPP). At 1, 4, 6, 8, 11, and 13 days after addition of PRP or PPP, the TGF-beta 1 and CTGF levels in supernatants were determined using solid-phase enzyme-linked immunosorbent assays. Quantitative reverse transcription polymerase chain reactions were performed to quantify TGF-beta 1 and CTGF mRNA expression levels. TGF-beta 1 mRNA expression in the PRP groups was lower than in the PPP groups from 4 to 13 days of culture, and there was statistically significant difference (P < .01). CTGF level and mRNA expression in the PRP groups was lower than in the PPP groups, and there were statistically significant differences (P < .01). Although further experiments will focus on clarifying the second messenger of the TGF-beta 1 negative feedback mechanism, the in vitro data presented show that PRP can potentially reduce CTGF and CTGF gene transcription by triggering the TGF-beta 1 signalling negative feedback mechanism.-
dc.format.extent8-
dc.language영어-
dc.language.isoENG-
dc.publisherBlackwell Publishing Inc.-
dc.titleThe effects of platelet-rich plasma on hypertrophic scars fibroblasts-
dc.typeArticle-
dc.publisher.location미국-
dc.identifier.doi10.1111/iwj.12896-
dc.identifier.scopusid2-s2.0-85055041778-
dc.identifier.wosid000440290900007-
dc.identifier.bibliographicCitationInternational Wound Journal, v.15, no.4, pp 547 - 554-
dc.citation.titleInternational Wound Journal-
dc.citation.volume15-
dc.citation.number4-
dc.citation.startPage547-
dc.citation.endPage554-
dc.type.docTypeArticle-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaDermatology-
dc.relation.journalResearchAreaSurgery-
dc.relation.journalWebOfScienceCategoryDermatology-
dc.relation.journalWebOfScienceCategorySurgery-
dc.subject.keywordPlusGROWTH-FACTOR-BETA-
dc.subject.keywordPlusGROWTH-FACTOR-BETA-1 MESSENGER-RNA-
dc.subject.keywordPlusNEUTRALIZING ANTIBODY-
dc.subject.keywordPlusGRANULATION-TISSUE-
dc.subject.keywordPlusWOUND CONTRACTION-
dc.subject.keywordPlusCOLLAGEN-MATRIX-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusPROTEIN-
dc.subject.keywordPlusSTIMULATION-
dc.subject.keywordPlusTGF-BETA(1)-
dc.subject.keywordAuthorcicatrix-
dc.subject.keywordAuthorconnective tissue growth factor-
dc.subject.keywordAuthorhypertrophic-
dc.subject.keywordAuthortransforming growth factor beta-
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