以C 型肝炎病毒感染模式研究Nur77與泌尿道發炎

之相關性

林大欽 Ta-Chin Lin, 鄭如茜 ( Ju-Chien Cheng)

三總醫院澎湖分院泌尿外科

Department of Urology, Tri-service General Hospital Penghu Branch

中國醫藥大學醫學檢驗生物技術學系

Department of Medical Laboratory Science and Biotechnology, China Medical University

Introduction: Persistent infection-caused inflammation leads to many diseases, including bladder and prostate cancer. Overexpression of Nur77, a nuclear transcriptional factor, was found to inhibit androgen-induced bladder cancer growth and prostate cancer proliferation.

Purpose: we use HCV as a model system to understand how nuclear exported-Nu77 inhibits inflammation and may apply to bladder and prostate-associated inflammation related disease.

Materials and Methods: Since Nur77 can be translocated to cytoplasm during HCV infection, we use HCV as a model system to observe the anti-inflammatory effect of cytoplasm-located Nur77. Western blotting and Immunofluorescence staining were applied to the study. 

Result: HCV infected Huh7.5.1 cells increased the expression level of Nur77 in cytoplasm. Since LBD domain of Nur77 interacts with HCV NSB. The LBD domain of Nur77 was transfected into Huh7.5.1 cells following infection with HCV. The LBD domain of Nur77 enhanced the expression of HCV NS3 and reduces the expression of p62 and phosphorylated-NF-κB.

Conclusion

The cytoplasmic shuttling Nur77 may inhibit NF-κB through autophagy-NF-κB axis. These data provide the possibility of early intervention in the patients with urinary tract related inflammation caused by overexpression of Nur77.