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The potential regulatory role of miR16 to the interplay between interferon and transforming growth factor beta pathways through IRF3 and SMAD7 in hepatitis C virus infected patients
Author(s) -
Hany Noha Mohamed,
Hammouda AbdElRahman M. A.,
Nabih Enas Samir,
Mohamed Sherif Moneir
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28537
Subject(s) - irf3 , interferon regulatory factors , virology , interferon , transforming growth factor beta , beta (programming language) , interferon beta , virus , transforming growth factor , biology , immunology , medicine , microbiology and biotechnology , immune system , computer science , innate immune system , programming language
Background The defensive strategy against hepatitis C virus (HCV) infection depends on two antiviral pathways; interferon (IFN) and transforming growth factor β (TGFβ). We aimed at verifying the relation between TGFβ and IFN antiviral pathways in HCV infection through SMAD7 and IRF3, and whether a possible regulatory role for microRNA‐16 (miR16) on the interplay between IFN and TGFβ signaling pathways exists or not. Methods We evaluated miR16, IRF3 and SMAD7 expression by real‐time polymerase chain reaction in HCV infected patients and age and gender matched healthy controls. Results miR16 expression was significantly higher while IRF3 and SMAD7 expression was significantly lower in HCV patients compared with healthy controls. Meanwhile, miR16 was negatively correlated to SMAD7 in HCV patients while IRF3 and SMAD7 were positively correlated. Conclusions The interplay between IFN and TGFβ pathways through IRF3 and SMAD7 in the context of immunity against HCV infection could be under the control of miR16.