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Cytokeratin 8 Was Over-Expressed in Cells Harboring in Vitro-Transcribed Full Length Hepatitis C Virus 1b RNA, but Down-Expressed in HCV Patients’ Serum

Received: 21 May 2014    Accepted: 16 June 2014    Published: 30 June 2014
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Abstract

Objectives: Previous proteome analysis conducted by our group has demonstrated that cytokeratin 8 was overexpressed in HuH-7 cells harboring in vitro transcribed HCV 1b full length RNA (HuH-7-HCV). Present study was aim to verify the results of proteomics, and obtain the clinical data of CK8 expresson levels in HCV patients. Methods: The expression level of CK 8 in HuH-7-HCV cells was examined by Real time PCR and Western blotting. The concentration of CK8 in HCV patients’ serum was measured by enzyme-linked immunosorbent assay (ELISA). Results: The results showed expression level of CK8 transcript in HuH-7-HCV cells was 2.3 fold higher than that in HuH-7 mock cells (P<0.01). The protein expression of CK8 in HuH-7-HCV cells was approximately 3 fold higher than that in HuH-7 mock cells (P<0.01). However, results of ELISA demonstrated the serum CK8 concentration was significantly reduced in chronic HCV patients compared to normal healthy controls (P<0.01). And there was a negative linear correlation between serum CK8 concentration and HCV RNA titer (r=-0.380, P<0.01). Conclusion: Our present study supports the hypothesis that in response to HCV infection, expression of CK8 was increased, which may contribute to the essential cytoprotection provided by CK8 in the liver. Altered CK8 expression pattern could be an important event in the pathogenesis of HCV infection. CK8 have potential use as surrogate markers of liver injury.

Published in Clinical Medicine Research (Volume 3, Issue 3)
DOI 10.11648/j.cmr.20140303.16
Page(s) 80-86
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This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Hepatitis C Virus, Cytokeratin 8, HuH-7-HCV, Serum, Expression Levels

References
[1] Ezzikouri, S., P. Pineau and S. Benjelloun, Hepatitis C virus infection in the Maghreb region. J Med Virol, 2013. 85(9): p. 1542-9.
[2] Lagging, M., et al., Retreatment with peg-interferon and ribavirin in patients with chronic hepatitis C virus genotype 2 or 3 infection with prior relapse. Scand J Gastroenterol, 2013. 48(7): p. 839-47.
[3] Xun, M., et al., Proteomic analysis of HuH-7 cells harboring in vitro-transcribed full-length hepatitis C virus 1b RNA. Acta Pharmacol Sin, 2008. 29(6): p. 720-7.
[4] Tang, H.L., et al., inventors; Yangling, Daiying Biolog Engine (CN), as-signee. The intact hepatitis C virus and the method for culturing it in in vitro cell culture. European Patent 1 424 390. 2004 Feb 06.
[5] Livak, K.J. and T.D. Schmittgen, Analysis of relative gene expression data using real-time quan-titative PCR and the 2(-Delta Delta C(T)) Method. Methods, 2001. 25(4): p. 402-8.
[6] Herrmann, H., et al., In-termediate filaments: primary determinants of cell architecture and plasticity. J Clin Invest, 2009. 119(7): p. 1772-83.
[7] Strnad, P., et al., Non-coding keratin variants associate with liver fibrosis progression in patients with hemochromatosis. PLoS One, 2012. 7(3): p. e32669.
[8] Omary, M.B., "IF-pathies": a broad spectrum of intermediate filament-associated diseases. J Clin Invest, 2009. 119(7): p. 1756-62.
[9] Iyer, S.V., et al., Under-standing the role of keratins 8 and 18 in neoplastic potential of breast cancer derived cell lines. PLoS One, 2013. 8(1): p. e53532.
[10] Usachov, V., et al., Keratin 8 variants are infrequent in patients with alcohol-related liver cirrhosis and do not associate with development of hepatocellular carcinoma. BMC Gastroenterol, 2012. 12: p. 147.
[11] Fortier, A.M., et al., Novel insights into changes in biochemical properties of keratins 8 and 18 in gri-seofulvin-induced toxic liver injury. Exp Mol Pathol, 2010. 89(2): p. 117-25.
[12] Omary, M.B., et al., Toward un-raveling the complexity of simple epithelial keratins in human disease. J Clin Invest, 2009. 119(7): p. 1794-805.
[13] Ku, N.O., et al., Keratins let liver live: Mutations predispose to liver disease and crosslinking ge-nerates Mallory-Denk bodies. Hepatology, 2007. 46(5): p. 1639-49.
[14] Zatloukal, K., et al., From Mallory to Mallory-Denk bodies: what, how and why? Exp Cell Res, 2007. 313(10): p. 2033-49.
[15] Kakehashi, A., et al., Cytokeratin 8/18 overexpression and complex formation as an indicator of GST-P positive foci transformation into hepatocellular carcinomas. Toxicol Appl Pharmacol, 2009. 238(1): p. 71-9.
[16] Kakehashi, A., et al., Cytokeratin 8/18 as a new marker of mouse liver preneoplastic lesions. Toxicol Appl Pharmacol, 2010. 242(1): p. 47-55.
[17] Zhong, B., et al., Keratin variants are overrepresented in primary biliary cirrhosis and associate with disease severity. Hepatology, 2009. 50(2): p. 546-54.
[18] Strnad, P., et al., Keratins: markers and modulators of liver disease. Curr Opin Gastroenterol, 2012. 28(3): p. 209-16.
[19] Strnad, P., et al., Keratin variants associate with progression of fibrosis during chronic hepatitis C infection. Hepatology, 2006. 43(6): p. 1354-63.
[20] Lee, J., et al., Predisposition to apoptosis in keratin 8-null liver is related to inactivation of NF-kappaB and SAPKs but not decreased c-Flip. Biol Open, 2013. 2(7): p. 695-702.
[21] Wang, Y., et al., Cytokeratin 8 silencing in human naso-pharyngeal carcinoma cells leads to cisplatin sensitization. Cancer Lett, 2008. 265(2): p. 188-96.
[22] Caulin, C., et al., Keratin-dependent, epithelial resistance to tumor necrosis factor-induced apoptosis. J Cell Biol, 2000. 149(1): p. 17-22.
[23] Gilbert, S., et al., Simple epithelium keratins 8 and 18 provide resistance to Fas-mediated apoptosis. The protection occurs through a receptor-targeting modulation. J Cell Biol, 2001. 154(4): p. 763-73.
[24] Fuentes-Gonzalez, A.M., et al., The modulation of apoptosis by oncogenic viruses. Virol J, 2013. 10: p. 182.
[25] Bantel, H. and K. Schulze-Osthoff, Apoptosis in hepatitis C virus infection. Cell Death Differ, 2003. 10 Suppl 1: p. S48-58.
[26] Valva, P., et al., Apoptosis markers related to pathogenesis of pediatric chronic hepatitis C virus infection: M30 mirrors the severity of steatosis. J Med Virol, 2010. 82(6): p. 949-57.
Cite This Article
  • APA Style

    Meng Xun, Haifeng Wang, Burong Li, Hongyan He, Qian He, et al. (2014). Cytokeratin 8 Was Over-Expressed in Cells Harboring in Vitro-Transcribed Full Length Hepatitis C Virus 1b RNA, but Down-Expressed in HCV Patients’ Serum. Clinical Medicine Research, 3(3), 80-86. https://doi.org/10.11648/j.cmr.20140303.16

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    ACS Style

    Meng Xun; Haifeng Wang; Burong Li; Hongyan He; Qian He, et al. Cytokeratin 8 Was Over-Expressed in Cells Harboring in Vitro-Transcribed Full Length Hepatitis C Virus 1b RNA, but Down-Expressed in HCV Patients’ Serum. Clin. Med. Res. 2014, 3(3), 80-86. doi: 10.11648/j.cmr.20140303.16

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    AMA Style

    Meng Xun, Haifeng Wang, Burong Li, Hongyan He, Qian He, et al. Cytokeratin 8 Was Over-Expressed in Cells Harboring in Vitro-Transcribed Full Length Hepatitis C Virus 1b RNA, but Down-Expressed in HCV Patients’ Serum. Clin Med Res. 2014;3(3):80-86. doi: 10.11648/j.cmr.20140303.16

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  • @article{10.11648/j.cmr.20140303.16,
      author = {Meng Xun and Haifeng Wang and Burong Li and Hongyan He and Qian He and Yonglie Chu},
      title = {Cytokeratin 8 Was Over-Expressed in Cells Harboring in Vitro-Transcribed Full Length Hepatitis C Virus 1b RNA, but Down-Expressed in HCV Patients’ Serum},
      journal = {Clinical Medicine Research},
      volume = {3},
      number = {3},
      pages = {80-86},
      doi = {10.11648/j.cmr.20140303.16},
      url = {https://doi.org/10.11648/j.cmr.20140303.16},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.cmr.20140303.16},
      abstract = {Objectives: Previous proteome analysis conducted by our group has demonstrated that cytokeratin 8 was overexpressed in HuH-7 cells harboring in vitro transcribed HCV 1b full length RNA (HuH-7-HCV). Present study was aim to verify the results of proteomics, and obtain the clinical data of CK8 expresson levels in HCV patients. Methods: The expression level of CK 8 in HuH-7-HCV cells was examined by Real time PCR and Western blotting. The concentration of CK8 in HCV patients’ serum was measured by enzyme-linked immunosorbent assay (ELISA). Results: The results showed expression level of CK8 transcript in HuH-7-HCV cells was 2.3 fold higher than that in HuH-7 mock cells (P<0.01). The protein expression of CK8 in HuH-7-HCV cells was approximately 3 fold higher than that in HuH-7 mock cells (P<0.01). However, results of ELISA demonstrated the serum CK8 concentration was significantly reduced in chronic HCV patients compared to normal healthy controls (P<0.01). And there was a negative linear correlation between serum CK8 concentration and HCV RNA titer (r=-0.380, P<0.01). Conclusion: Our present study supports the hypothesis that in response to HCV infection, expression of CK8 was increased, which may contribute to the essential cytoprotection provided by CK8 in the liver. Altered CK8 expression pattern could be an important event in the pathogenesis of HCV infection. CK8 have potential use as surrogate markers of liver injury.},
     year = {2014}
    }
    

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  • TY  - JOUR
    T1  - Cytokeratin 8 Was Over-Expressed in Cells Harboring in Vitro-Transcribed Full Length Hepatitis C Virus 1b RNA, but Down-Expressed in HCV Patients’ Serum
    AU  - Meng Xun
    AU  - Haifeng Wang
    AU  - Burong Li
    AU  - Hongyan He
    AU  - Qian He
    AU  - Yonglie Chu
    Y1  - 2014/06/30
    PY  - 2014
    N1  - https://doi.org/10.11648/j.cmr.20140303.16
    DO  - 10.11648/j.cmr.20140303.16
    T2  - Clinical Medicine Research
    JF  - Clinical Medicine Research
    JO  - Clinical Medicine Research
    SP  - 80
    EP  - 86
    PB  - Science Publishing Group
    SN  - 2326-9057
    UR  - https://doi.org/10.11648/j.cmr.20140303.16
    AB  - Objectives: Previous proteome analysis conducted by our group has demonstrated that cytokeratin 8 was overexpressed in HuH-7 cells harboring in vitro transcribed HCV 1b full length RNA (HuH-7-HCV). Present study was aim to verify the results of proteomics, and obtain the clinical data of CK8 expresson levels in HCV patients. Methods: The expression level of CK 8 in HuH-7-HCV cells was examined by Real time PCR and Western blotting. The concentration of CK8 in HCV patients’ serum was measured by enzyme-linked immunosorbent assay (ELISA). Results: The results showed expression level of CK8 transcript in HuH-7-HCV cells was 2.3 fold higher than that in HuH-7 mock cells (P<0.01). The protein expression of CK8 in HuH-7-HCV cells was approximately 3 fold higher than that in HuH-7 mock cells (P<0.01). However, results of ELISA demonstrated the serum CK8 concentration was significantly reduced in chronic HCV patients compared to normal healthy controls (P<0.01). And there was a negative linear correlation between serum CK8 concentration and HCV RNA titer (r=-0.380, P<0.01). Conclusion: Our present study supports the hypothesis that in response to HCV infection, expression of CK8 was increased, which may contribute to the essential cytoprotection provided by CK8 in the liver. Altered CK8 expression pattern could be an important event in the pathogenesis of HCV infection. CK8 have potential use as surrogate markers of liver injury.
    VL  - 3
    IS  - 3
    ER  - 

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Author Information
  • Department of Immunology and Microbiology, Medical School of Xi’an Jiaotong University, Xi’an, Shannxi, China

  • Department of Clinical Laboratories, Xi’an Central Hospital, Xi’an, Shannxi, China

  • Department of Clinical Laboratories, Second Affiliated Hospital of Medical School of Xi’an Jiaotong University, Xi’an, Shannxi, China

  • Department of Medical Technology, Xi’an Medical College, Xi’an, Shannxi, China

  • Department of Clinical Laboratories, Second Affiliated Hospital of Medical School of Xi’an Jiaotong University, Xi’an, Shannxi, China

  • Department of Immunology and Microbiology, Medical School of Xi’an Jiaotong University, Xi’an, Shannxi, China

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