Startseite Hepatitis B virus surface protein-induced hPIAS1 transcription requires TAL1, E47, MYOG, NFI, and MAPK signal pathways
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Hepatitis B virus surface protein-induced hPIAS1 transcription requires TAL1, E47, MYOG, NFI, and MAPK signal pathways

  • Hongyan Wang , Di Wu , Xiaofeng Wang , Guang Chen , Yuanya Zhang , Weiming Yan , Xiaoping Luo , Meifang Han EMAIL logo und Qin Ning EMAIL logo
Veröffentlicht/Copyright: 7. Juni 2016

Abstract

The protein inhibitor of activated STAT1 (PIAS1) plays important roles in regulating virus-induced chronic hepatitis, but the interaction between hepatitis B virus (HBV) and hPIAS1 is not clear. Our aim was to verify if HBV encoding proteins enhance the transcription of hPIAS1 and which cis-elements and transcription factors were involved in the mechanism. In order to do, so a series of molecular biological methods, along with functional and histological studies, were performed. We found that the HBV surface protein (HBs) enhanced hPIAS1 transcription through the activities of TAL1, E47, myogenin (MYOG), and NFI, dependent on the activation of p38MAPK and ERK signaling pathways in vitro, which might contribute to the ineffectiveness of treatment in CHB patients. Furthermore, liver samples from patients with high HBsAg levels and HBV DNA displayed increased hPIAS1 expression and high levels of TAL1, E47, MYOG, and NFI, compared to those patients with low HBsAg levels and HBV DNA, and healthy controls. These findings suggest that the HBs protein-induced hPIAS1 transcription requires TAL1, E47, MYOG, NFI, and MAPK signal pathways. It provides new potential targets for antiviral therapeutic strategies for controlling HBV-associated diseases.

Acknowledgments

We thank Jinshang Hu for secretarial assistance during the preparation of the manuscript. We also thank Editage colleague (Shanghai, China) for their language edits. This work was funded by the National Science Fund of China Grants (Grant NO. 81171558 and 81271808) and the Program for Innovative Research Team of Chinese Ministry of Education (IRT14 R20).

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Supplemental Material:

The online version of this article (DOI: 10.1515/hsz-2015-0290) offers supplementary material, available to authorized users.


Received: 2015-11-27
Accepted: 2016-6-6
Published Online: 2016-6-7
Published in Print: 2016-11-1

©2016 Walter de Gruyter GmbH, Berlin/Boston

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