JaLCDOI 10.18926/AMO/54190
フルテキストURL 70_2_111.pdf
著者 Takeda, Midori| Ikeda, Masanori| Satoh, Shinya| Dansako, Hiromichi| Wakita, Takaji| Kato, Nobuyuki|
抄録 Membrane transport probably participates in the lifecycle of hepatitis C virus (HCV). Rab proteins are essential host factors for HCV RNA replication, but these proteins’ roles in other steps of the HCV lifecycle are not clear. The tight junction (TJ) plays a key role in HCV infection. Rab13 regulates the endocytic recycling of the TJ-associated proteins. Here we investigated whether Rab13 is involved in the HCV entry step. We used HuH-7-derived RSc cells and Li23-derived D7 cells. To evaluate the effect of Rab13 in HCV infection, we transfected the cells with siRNA targeting Rab13 before HCV infection. The down-regulation of Rab13 inhibited HCV infection. The D7 cells had showed a greater inhibitory effect against HCV infection compared to that in the RSc cells by Rab13 knockdown. Next, to evaluate the effect of Rab13 after infection, we inoculated the cells with HCV before transfection of the siRNA. The down-regulation of Rab13 did not show any effects after HCV infection. We further examined whether Rab13 would influence HCV RNA replication by using HCV replicon-harboring cells. The results revealed that Rab13 did not affect the step of HCV RNA replication. These results suggest that Rab13 plays an important role in the step of HCV entry.
キーワード hepatitis C virus Rab13 occludin claudin 1
Amo Type Original Article
発行日 2016-04
出版物タイトル Acta Medica Okayama
70巻
2号
出版者 Okayama University Medical School
開始ページ 111
終了ページ 118
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
著作権者 CopyrightⒸ 2016 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 27094836
Web of Sience KeyUT 000377626300006
JaLCDOI 10.18926/AMO/54186
フルテキストURL 70_2_75.pdf
著者 Sejima, Hiroe| Satoh, Shinya| Dansako, Hiromichi| Honda, Masao| Kaneko, Shuichi| Ikeda, Masanori| Kato, Nobuyuki|
抄録 The mechanisms of hepatitis C virus (HCV)-associated hepatocarcinogenesis and disease progression are unclear. We previously observed that the expression level of carboxypeptidase B2 (CPB2) gene was remarkably suppressed by persistent HCV RNA replication in human hepatoma cell line Li23-derived cells. The results of the present study demonstrated that the CPB2 expression in patients with chronic hepatitis C was inversely correlated with several risk factors of hepatic fibrosis or steatosis, although ectopic CPB2 expression did not suppress the expression of fibrogenic or lipogenic genes. The suppressed CPB2 expression was restored by treatment with 5-azacytidine. To clarify the mechanism underlying this phenomenon, we analyzed the CPB2 promoter, and the results revealed that (1) hepatocyte nuclear factor 1 (HNF1), especially HNF1α, was essential for the CPB2 promoter, and (2) CPB2 promoter was not methylated by persistent HCV RNA replication. The expression levels of HNF1α and HNF1β were also not changed by persistent HCV RNA replication. These results suggest the existence of 5-azacytidine-inducible or -reducible unknown factor(s) that can control the CPB2 expression. To evaluate this idea we performed a microarray analysis, and several gene candidates corresponding to the suggested factor(s) were identified.
キーワード persistent hepatitis C virus replication carboxypeptidase B2 suppression mechanism of CPB2 expression DNA methylation hepatocyte nuclear factor 1
Amo Type Original Article
発行日 2016-04
出版物タイトル Acta Medica Okayama
70巻
2号
出版者 Okayama University Medical School
開始ページ 75
終了ページ 88
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
著作権者 CopyrightⒸ 2016 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 27094832
Web of Sience KeyUT 000377626300002