Interferon-alpha Induces High Expression of APOBEC3G and STAT-1 in Vitro and in VivoReport as inadecuate




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Department of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan 430060, China





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Abstract To investigate whether the JAK-STAT Janus kinase-signal transducers and activators of transcription pathway participates in the regulation of APOBEC3G Apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like 3G gene transcription and to study the molecular mechanisms of interferon resistance in patients with chronic hepatitis B CHB, changes in APOBEC3G and STAT-1 expression levels in HepG2.2.15 cells after treatment with various concentrations of IFN-a, were detected using real-time RT-PCR and Western-blot. In addition, the differences in STAT-1 and APOBEC3G expression in liver tissues were also observed in patients with different anti-viral responses to IFN-a. It is found that IFN-a suppressed HBV replication and expression markedly in HepG2.2.15 cells, and simultaneously enhanced APOBEC3G expression in a dose- or time-dependent manner within a certain range. Moreover, a corresponding gradual increase in STAT-1 expression levels was also observed. The expression levels of STAT-1 and APOBEC3G in the liver of CHB patients with a complete response to IFN-a are significantly higher than that of the patients with non-response to IFN-a treatment. It is suggested that inducing intracellular APOBEC3G expression may be one of anti-HBV mechanisms of IFN-a, and IFN-a-induced APOBEC3G expression may be via the JAK-STAT signaling pathway. Moreover, interferon resistance may be related to the down-regulation of STAT-1 expression in the patients who had non-response to IFN-a treatment. View Full-Text

Keywords: STAT-1; interferon-alpha; APOBEC3G; HepG2.2.15 cell; chronic hepatitis B STAT-1; interferon-alpha; APOBEC3G; HepG2.2.15 cell; chronic hepatitis B





Author: Hui Chen, Lu-Wen Wang, Yan-Qing Huang and Zuo-Jiong Gong *

Source: http://mdpi.com/



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