丙型肝炎病毒诱导纤维化体外模型的建立

IF 2.1 4区医学 Q3 VIROLOGY

Future Virology Pub Date : 2023-09-08 DOI:10.2217/fvl-2022-0206

Bisma Rauff, Mehdi Ramezani-Moghadam, Enoch S. E. Tay, Jacob George, M. Douglas

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引用次数: 0

摘要

目的:建立慢性丙型肝炎病毒(HCV)感染肝纤维化的体外模型，探讨其发生机制。方法:用HCV (JFH1或Jc1)或亚基因组复制子转染Huh7细胞，用qPCR检测促纤维化细胞因子的表达。将感染细胞的培养基转移到LX2细胞或原代大鼠星状细胞上，用qPCR检测促纤维化基因的表达。结果:可复制的HCV可诱导TGF-β1和CTGF的表达，而亚基因组复制子则不能。感染细胞的上清液诱导α-SMA和COL1A1表达和星状细胞迁移，证实功能激活。结论:感染细胞产生促纤维化因子TGF-β1和CTGF，活化星状细胞。这一机制可用于预防或治疗丙型肝炎病毒诱导的纤维化。

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Development of an in vitro model to study hepatitis C virus-induced fibrosis

Aim: To investigate the mechanism of liver fibrosis in chronic hepatitis C virus (HCV) infection we developed an in vitro model. Methods: Huh7 cells were transfected with HCV (JFH1 or Jc1) or sub-genomic replicons and expression of pro-fibrotic cytokines determined by qPCR. Media from infected cells was transferred onto LX2 cells or primary rat stellate cells and expression of pro-fibrotic genes measured by qPCR. Results: Replication competent HCV, but not sub-genomic replicons, induced expression of TGF-β1 and CTGF. Supernatant from infected cells induced α-SMA and COL1A1 expression and stellate cell migration, confirming functional activation. Conclusion: Infected cells produce pro-fibrogenic cytokines TGF-β1 and CTGF and activate stellate cells. This mechanism could be targeted to prevent or treat HCV-induced fibrosis.

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来源期刊

Future Virology 医学-病毒学

CiteScore

4.00

自引率

3.20%

发文量

审稿时长

6-12 weeks

期刊介绍： Future Virology is a peer-reviewed journal that delivers essential information in concise, at-a-glance article formats. Key advances in the field are reported and analyzed by international experts, providing an authoritative but accessible forum for this ever-expanding area of research. It is an interdisciplinary forum for all scientists working in the field today.