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  • Wiley  (3)
  • Zheng, Jianjian  (3)
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  • Wiley  (3)
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  • 1
    Online Resource
    Online Resource
    Salvianolic acid B‐induced micro RNA ‐152 inhibits liver fibrosis by attenuating DNMT 1‐mediated Patched1 methylation
    Wiley ; 2015
    In:  Journal of Cellular and Molecular Medicine Vol. 19, No. 11 ( 2015-11), p. 2617-2632
    Details
    In: Journal of Cellular and Molecular Medicine, Wiley, Vol. 19, No. 11 ( 2015-11), p. 2617-2632
    Abstract: Epithelial‐mesenchymal transition ( EMT ) was reported to be involved in the activation of hepatic stellate cells ( HSC s), contributing to the development of liver fibrosis. Epithelial‐mesenchymal transition can be promoted by the Hedgehog (Hh) pathway. Patched1 ( PTCH 1), a negative regulatory factor of the Hh signalling pathway, was down‐regulated during liver fibrosis and associated with its hypermethylation status. Micro RNA s (mi RNA s) are reported to play a critical role in the control of various HSC s functions. However, mi RNA ‐mediated epigenetic regulations in EMT during liver fibrosis are seldom studied. In this study, Salvianolic acid B (Sal B) suppressed the activation of HSC s in CC l 4 ‐treated mice and mouse primary HSC s, leading to inhibition of cell proliferation, type I collagen and alpha‐smooth muscle actin. We demonstrated that the antifibrotic effects caused by Sal B were, at least in part, via inhibition of EMT and the Hh pathway. In particular, up‐regulation of PTCH 1 was associated with decreased DNA methylation level after Sal B treatment. Accordingly, DNA methyltransferase 1 ( DNMT 1) was attenuated by Sal B in vivo and in vitro . The knockdown of DNMT 1 in Sal B‐treated HSC s enhanced PTCH 1 expression and its demethylation level. Interestingly, increased miR‐152 in Sal B‐treated cells was responsible for the hypomethylation of PTCH 1 by Sal B. As confirmed by the luciferase activity assay, DNMT 1 was a direct target of miR‐152. Further studies showed that the miR‐152 inhibitor reversed Sal B‐mediated PTCH 1 up‐regulation and DNMT 1 down‐regulation. Collectively, miR‐152 induced by Sal B, contributed to DNMT 1 down‐regulation and epigenetically regulated PTCH 1, resulting in the inhibition of EMT in liver fibrosis.
    Type of Medium: Online Resource
    ISSN: 1582-1838 , 1582-4934
    URL: Issue
    URL: Article
    DOI: 10.1111/jcmm.2015.19.issue-11
    DOI: 10.1111/jcmm.12655
    Language: English
    Publisher: Wiley
    Publication Date: 2015
    detail.hit.zdb_id: 2076114-4
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  • 2
    Online Resource
    Online Resource
    linc RNA ‐p21 inhibits hepatic stellate cell activation and liver fibrogenesis via p21
    Wiley ; 2015
    In:  The FEBS Journal Vol. 282, No. 24 ( 2015-12), p. 4810-4821
    Details
    In: The FEBS Journal, Wiley, Vol. 282, No. 24 ( 2015-12), p. 4810-4821
    Abstract: Long non‐coding RNA s are involved in various biological processes and diseases. The biological role of long intergenic non‐coding RNA ‐p21 (linc RNA ‐p21) in liver fibrosis remains unknown before this study. In this study, we observed marked reduction of linc RNA ‐p21 expression in mice liver fibrosis models and human cirrhotic liver. Over‐expression of linc RNA ‐p21 suppressed activation of hepatic stellate cells ( HSC s) in vitro . Lentivirus‐mediated linc RNA ‐p21 transfer into mice decreased the severity of liver fibrosis in vivo . Additionally, linc RNA ‐p21 reversed the activation of HSC s to their quiescent phenotype. The mRNA levels of linc RNA ‐p21 and p21 were positively correlated. Our results show that over‐expression of linc RNA ‐p21 promotes up‐regulation of p21 at both the mRNA and protein levels. Furthermore, linc RNA ‐p21 inhibited cell‐cycle progression and proliferation of primary HSC s through enhancement of p21 expression. Compared with healthy subjects, serum linc RNA ‐p21 levels were significantly lower in patients with liver cirrhosis, especially those with decompensation. These findings collectively indicate that linc RNA ‐p21 is a mediator of HSC activation, supporting its utility as a novel therapeutic target for liver fibrosis.
    Type of Medium: Online Resource
    ISSN: 1742-464X , 1742-4658
    URL: Issue
    URL: Article
    DOI: 10.1111/febs.2015.282.issue-24
    DOI: 10.1111/febs.13544
    Language: English
    Publisher: Wiley
    Publication Date: 2015
    detail.hit.zdb_id: 2172518-4
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Curcumin up‐regulates phosphatase and tensin homologue deleted on chromosome 10 through micro RNA ‐mediated control of DNA methylation – a novel mechanism suppressing liver fibrosis
    Wiley ; 2014
    In:  The FEBS Journal Vol. 281, No. 1 ( 2014-01), p. 88-103
    Details
    In: The FEBS Journal, Wiley, Vol. 281, No. 1 ( 2014-01), p. 88-103
    Abstract: Phosphatase and tensin homologue deleted on chromosome 10 ( PTEN ) has been reported to play a role in the suppression of activated hepatic stellate cells ( HSC s). Moreover, it has been demonstrated that hypermethylation of the PTEN promoter is responsible for the loss of PTEN expression during HSC activation. Methylation is now established as a fundamental regulator of gene transcription. Micro RNA s (mi RNA s), which can control gene expression by binding to their target genes for degradation and/or translational repression, were found to be involved in liver fibrosis. However, the mechanism responsible for mi RNA ‐mediated epigenetic regulation in liver fibrosis still remained unclear. In the present study, curcumin treatment significantly resulted in the inhibition of cell proliferation and an increase in the apoptosis rate through the up‐regulation of PTEN associated with a decreased DNA methylation level. Only DNA methyltransferase 3b ( DNMT 3b) was reduced in vivo and in vitro after curcumin treatment. Further studies were performed aiming to confirm that the knockdown of DNMT 3b enhanced the loss of PTEN methylation by curcumin. In addition, miR‐29b was involved in the hypomethylation of PTEN by curcumin. MiR‐29b not only was increased by curcumin in activated HSC s, but also was confirmed to target DNMT 3b by luciferase activity assays. Curcumin‐mediated PTEN up‐regulation, DNMT 3b down‐regulation and PTEN hypomethylation were all attenuated by miR‐29b inhibitor. Collectively, it is demonstrated that curcumin can up‐regulate miR‐29b expression, resulting in DNMT 3b down‐regulation in HSC s and epigenetically‐regulated PTEN involved in the suppression of activated HSC s. These results indicate that mi RNA ‐mediated epigenetic regulation may be a novel mechanism suppressing liver fibrosis.
    Type of Medium: Online Resource
    ISSN: 1742-464X , 1742-4658
    URL: Issue
    URL: Article
    DOI: 10.1111/febs.2013.281.issue-1
    DOI: 10.1111/febs.12574
    Language: English
    Publisher: Wiley
    Publication Date: 2014
    detail.hit.zdb_id: 2172518-4
    SSG: 12
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