HCV/Oxidative Stress and Liver Disease by Michiari Okuda, Lori A. Showalter, Kazuhiro Otani (auth.),

By Michiari Okuda, Lori A. Showalter, Kazuhiro Otani (auth.), Kiwamu Okita M.D., Ph.D. (eds.)

Since the invention of superoxide dismutase greater than 3 a long time in the past, there was fast progress within the wisdom of oxidative pressure and illness. This quantity containing the court cases of the thirteenth Yamaguchi Symposium on Liver disorder comprises dialogue of the direct mobile results of hepatitis C virus (HCV) proteins on hepatocytes and experiences proof that oxidative pressure triggered basically by way of the HCV center protein performs a key function in ailment pathogenesis. additionally incorporated are chapters on new features of oxidative rigidity and liver illness resembling carbon monoxide as a regulator of liver microcirculation, hepatic iron accumulation and the prevalence of hepatocellular carcinoma, and oxidative rigidity within the absence of irritation in hepatocarcinogenesis. This number of papers from the Yamaguchi Symposium creates a necessary reference source for physicians and hepatologists.

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As shown in Fig. 6A, HCV core protein was detected in the immunoprecipitates by using JAKI and JAK2 antibodies, but not in that using the rabbit nonspecific y-globulin. This strongly suggests the binding of HCV core protein to the JAK proteins. Similar results were also seen in samples from 1L-6- and 1FN-y-treated cells, indicating that the binding of HCV core protein to the JAK proteins can occur irrespective of the phosphorylation status of JAK. HCV Core Protein Enhances Cytokine Receptor Expression We also investigated the influence of HCV core protein on expression of cytokine receptor mRNAs.

As for the role of IFN-y, it is believed to be closely associated with both virus eradication from the liver and the development of hepatitis. Taken together, HCV core-mediated modulation on the cell cycle machinery and the JAK -STAT signaling pathway may substantially contribute to the pathogenesis of HCV-related liver diseases. References 1. Hijikata M, Mizushima H, Tanji Y, Komoda Y, Hirowatari Y, Akagi T, Kato N, Kimura K, Shimotohno K (1993) Proteolytic processing and membrane association of putative nonstructural proteins of hepatitis C virus.

The difference in the data may be because regulation of bel-xl expression appears to be quite complex and the contribution of NFKB to this process may depend on cell type or activating stimuli. In fact, other studies failed to reveal alterations in bel-xl transcript levels by NFKB activation [28]. On the contrary, it was reported that NFKB activation was a negative regulator of BclXL in double-positive thymocytes [29]. Thus, further study is needed to clarify the fine regulation of Bcl-xL expression by NFKB.

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