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RSJYB1 inhibits collagen type I protein expression in hepatic stellate cells via down-regulating activity of collagen ?1 (I) promoter.

ABSTRACT: YB1 is a negative regulator in liver fibrosis. We wondered whether SJYB1, a homologous protein of YB1 from Schistosoma japonicum, has an effect on liver fibrosis in vitro. Recombinant SJYB1 (rSJYB1) protein was expressed in a bacterial system and purified by Ni-NTA His·Bind Resin. A human hepatic stellate cell line, the LX-2 cell line, was cultured and treated with rSJYB1. The role of rSJYB1 on LX-2 cells was then analysed by Western blot and luciferase assay. We succeeded in expressing and purifying SJYB1 in a bacterial system and the purified rSJYB1 could be recognized by S japonicum-infected rabbit sera. Western bolt analysis showed that rSJYB1 inhibited the expression of collagen type I, but had little effect on ?-smooth muscle actin (?-SMA). Further analysis revealed that rSJYB1 inhibited the activity of collagen ?1 (I) (COL1A1) promoter and functioned at -1592/-1176 region of COL1A1 promoter. Our data demonstrate that rSJYB1-mediated anti-fibrotic activity involves inhibiting the activity of COL1A1 promoter and subsequently suppressing the expression of collagen type I in hepatic stellate cells.

SUBMITTER: Chen L

PROVIDER: S-EPMC6484296 | biostudies-literature | 2019 May

REPOSITORIES: biostudies-literature

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rSJYB1 inhibits collagen type I protein expression in hepatic stellate cells via down-regulating activity of collagen α1 (I) promoter.

Chen Liuting L Ji Zhaodong Z Duan Lian L Zhu Dandan D Chen Jinling J Sun Xiaolei X Yu Yang Y Duan Yinong Y

Journal of cellular and molecular medicine 20190320 5

YB1 is a negative regulator in liver fibrosis. We wondered whether SJYB1, a homologous protein of YB1 from Schistosoma japonicum, has an effect on liver fibrosis in vitro. Recombinant SJYB1 (rSJYB1) protein was expressed in a bacterial system and purified by Ni-NTA His·Bind Resin. A human hepatic stellate cell line, the LX-2 cell line, was cultured and treated with rSJYB1. The role of rSJYB1 on LX-2 cells was then analysed by Western blot and luciferase assay. We succeeded in expressing and puri ...[more]

PMID: 30895719

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Project description:BackgroundIn chronic liver disease, hepatic stellate cells (HSC) transdifferentiate into myofibroblasts, promoting extracellular matrix (ECM) synthesis and deposition. Stimulation of HSC by transforming growth factor-? (TGF-?) is a crucial event in liver fibrogenesis due to its impact on myofibroblastic transition and ECM induction. In contrast, hepatocyte growth factor (HGF), exerts antifibrotic activities. Recently, miR-29 has been reported to be involved in ECM synthesis. We therefore studied the influence of HGF and TGF-? on the miR-29 collagen axis in HSC.MethodologyHSC, isolated from rats, were characterized for HGF and Met receptor expression by Real-Time PCR and Western blotting during culture induced myofibroblastic transition. Then, the levels of TGF-?, HGF, collagen-I and -IV mRNA, in addition to miR-29a and miR-29b were determined after HGF and TGF-? stimulation of HSC or after experimental fibrosis induced by bile-duct obstruction in rats. The interaction of miR-29 with 3'-untranslated mRNA regions (UTR) was analyzed by reporter assays. The repressive effect of miR-29 on collagen synthesis was studied in HSC treated with miR-29-mimicks by Real-Time PCR and immunoblotting.Principal findingsThe 3'-UTR of the collagen-1 and -4 subtypes were identified to bind miR-29. Hence, miR-29a/b overexpression in HSC resulted in a marked reduction of collagen-I and -IV synthesis. Conversely, a decrease in miR-29 levels is observed during collagen accumulation upon experimental fibrosis, in vivo, and after TGF-? stimulation of HSC, in vitro. Finally, we show that during myofibroblastic transition and TGF-? exposure the HGF-receptor, Met, is upregulated in HSC. Thus, whereas TGF-? stimulation leads to a reduction in miR-29 expression and de-repression of collagen synthesis, stimulation with HGF was definitely associated with highly elevated miR-29 levels and markedly repressed collagen-I and -IV synthesis.ConclusionsUpregulation of miRNA-29 by HGF and downregulation by TGF-? take part in the anti- or profibrogenic response of HSC, respectively.

Dataset Information

RSJYB1 inhibits collagen type I protein expression in hepatic stellate cells via down-regulating activity of collagen ?1 (I) promoter.

Publications

rSJYB1 inhibits collagen type I protein expression in hepatic stellate cells via down-regulating activity of collagen α1 (I) promoter.

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