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dc.contributor.authorYang, MF
dc.contributor.authorXie, J
dc.contributor.authorGu, XY
dc.contributor.authorZhang, XH
dc.contributor.authorDavey, AK
dc.contributor.authorZhang, SJ
dc.contributor.authorWang, JP
dc.contributor.authorZhu, RM
dc.date.accessioned2017-05-03T14:05:57Z
dc.date.available2017-05-03T14:05:57Z
dc.date.issued2009
dc.date.modified2011-08-31T07:19:23Z
dc.identifier.issn1007-9327
dc.identifier.doi10.3748/wjg.15.2109
dc.identifier.urihttp://hdl.handle.net/10072/40550
dc.description.abstractAIM: To investigate the relationship between 90-kuD ribosomal S6 kinase (p90RSK) and collagen type I expression during the development of hepatic fibrosis in vivo and in vitro.METHODS: Rat hepatic fibrosis was induced by intraperitoneal injection of dimethylnitrosamine. The protein expression and cell location of p90RSK and their relationship with collagen type I were determined by co-immunofluoresence and confocal microscopy. Subsequently, RNAi strategy was employed to silence p90RSK mRNA expression in HSC-T6, an activated hepatic stellate cell (HSC) line. The expression of collagen type I in HSC-T6 cells was assessed by Western blotting and real-time polymerase chain reaction. Furthermore, HSCs were transfected with expression vectors or RNAi constructs of p90RSK to increase or decrease the p90RSK expression, then collagen type I promoter activity in the transfected HSCs was examined by reporter assay. Lastly HSC-T6 cells transfected with p90RSK siRNA was treated with or without platelet-derived growth factor (PDGF)-BB at a final concentration of 20 姯L and the cell growth was determined by MTS conversion.RESULTS: In fibrotic liver tissues, p90RSK was over-expressed in activated HSCs and had a significant positive correlation with collagen type I levels. In HSC-T6 cells transfected with RNAi targeted to p90RSK, the expression of collagen type I was down-regulated (61.8% in mRNA, P < 0.01, 89.1% in protein, P < 0.01). However, collagen type I promoter activity was not increased with over-expression of p90RSK and not decreased with low expression either, compared with controls in the same cell line (P = 0.076). Furthermore, p90RSK siRNA exerted the inhibition of HSC proliferation, and also abolished the effect of PDGF on the HSC proliferation.CONCLUSION: p90RSK is over-expressed in activated HSCs and involved in regulating the abnormal expression of collagen type I through initiating the proliferation of HSCs.
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.languageeng
dc.language.isoen_AU
dc.publisherBeijing Baishideng BioMed Scientific Co., Ltd
dc.publisher.placeChina
dc.relation.ispartofstudentpublicationN
dc.relation.ispartofpagefrom2109
dc.relation.ispartofpageto2115
dc.relation.ispartofissue17
dc.relation.ispartofjournalWorld Journal of Gastroenterology
dc.relation.ispartofvolume15
dc.rights.retentionY
dc.subject.fieldofresearchBasic Pharmacology
dc.subject.fieldofresearchClinical Sciences
dc.subject.fieldofresearchcode111501
dc.subject.fieldofresearchcode1103
dc.titleInvolvement of 90-kuD ribosomal S6 kinase in collagen type I expression in rat hepatic fibrosis
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.rights.copyrightSelf-archiving of the author-manuscript version is not yet supported by this journal. Please refer to the journal link for access to the definitive, published version or contact the author[s] for more information.
gro.date.issued2009
gro.hasfulltextNo Full Text
gro.griffith.authorDavey, Andrew


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