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Article

Analysis of mitochondrial transcription factor A SNPs in alcoholic cirrhosis

  • Authors:
    • Chun Tang
    • Hongming Liu
    • Yongliang Tang
    • Yong Guo
    • Xianchun Liang
    • Liping Guo
    • Ruxian Pi
    • Juntao Yang
  • View Affiliations / Copyright

    Affiliations: Department of Hepatobiliary Surgery, Daping Hospital and Research Institute of Surgery, Third Military Medical University, Chongqing 400042, P.R. China
  • Pages: 73-79
    |
    Published online on: October 21, 2013
       https://doi.org/10.3892/etm.2013.1353
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Abstract

Genetic susceptibility to alcoholic cirrhosis (AC) exists. We previously demonstrated hepatic mitochondrial DNA (mtDNA) damage in patients with AC compared with chronic alcoholics without cirrhosis. Mitochondrial transcription factor A (mtTFA) is central to mtDNA expression regulation and repair; however, it is unclear whether there are specific mtTFA single nucleotide polymorphisms (SNPs) in patients with AC and whether they affect mtDNA repair. In the present study, we screened mtTFA SNPs in patients with AC and analyzed their impact on the copy number of mtDNA in AC. A total of 50 patients with AC, 50 alcoholics without AC and 50 normal subjects were enrolled in the study. SNPs of full‑length mtTFA were analyzed using the polymerase chain reaction (PCR) combined with gene sequencing. The hepatic mtTFA mRNA and mtDNA copy numbers were measured using quantitative PCR (qPCR), and mtTFA protein was measured using western blot analysis. A total of 18 mtTFA SNPs specific to patients with AC with frequencies >10% were identified. Two were located in the coding region and 16 were identified in non‑coding regions. Conversely, there were five SNPs that were only present in patients with AC and normal subjects and had a frequency >10%. In the AC group, the hepatic mtTFA mRNA and protein levels were significantly lower than those in the other two groups. Moreover, the hepatic mtDNA copy number was significantly lower in the AC group than in the controls and alcoholics without AC. Based on these data, we conclude that AC‑specific mtTFA SNPs may be responsible for the observed reductions in mtTFA mRNA, protein levels and mtDNA copy number and they may also increase the susceptibility to AC.
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Copy and paste a formatted citation
Spandidos Publications style
Tang C, Liu H, Tang Y, Guo Y, Liang X, Guo L, Pi R and Yang J: Analysis of mitochondrial transcription factor A SNPs in alcoholic cirrhosis. Exp Ther Med 7: 73-79, 2014.
APA
Tang, C., Liu, H., Tang, Y., Guo, Y., Liang, X., Guo, L. ... Yang, J. (2014). Analysis of mitochondrial transcription factor A SNPs in alcoholic cirrhosis. Experimental and Therapeutic Medicine, 7, 73-79. https://doi.org/10.3892/etm.2013.1353
MLA
Tang, C., Liu, H., Tang, Y., Guo, Y., Liang, X., Guo, L., Pi, R., Yang, J."Analysis of mitochondrial transcription factor A SNPs in alcoholic cirrhosis". Experimental and Therapeutic Medicine 7.1 (2014): 73-79.
Chicago
Tang, C., Liu, H., Tang, Y., Guo, Y., Liang, X., Guo, L., Pi, R., Yang, J."Analysis of mitochondrial transcription factor A SNPs in alcoholic cirrhosis". Experimental and Therapeutic Medicine 7, no. 1 (2014): 73-79. https://doi.org/10.3892/etm.2013.1353
Copy and paste a formatted citation
x
Spandidos Publications style
Tang C, Liu H, Tang Y, Guo Y, Liang X, Guo L, Pi R and Yang J: Analysis of mitochondrial transcription factor A SNPs in alcoholic cirrhosis. Exp Ther Med 7: 73-79, 2014.
APA
Tang, C., Liu, H., Tang, Y., Guo, Y., Liang, X., Guo, L. ... Yang, J. (2014). Analysis of mitochondrial transcription factor A SNPs in alcoholic cirrhosis. Experimental and Therapeutic Medicine, 7, 73-79. https://doi.org/10.3892/etm.2013.1353
MLA
Tang, C., Liu, H., Tang, Y., Guo, Y., Liang, X., Guo, L., Pi, R., Yang, J."Analysis of mitochondrial transcription factor A SNPs in alcoholic cirrhosis". Experimental and Therapeutic Medicine 7.1 (2014): 73-79.
Chicago
Tang, C., Liu, H., Tang, Y., Guo, Y., Liang, X., Guo, L., Pi, R., Yang, J."Analysis of mitochondrial transcription factor A SNPs in alcoholic cirrhosis". Experimental and Therapeutic Medicine 7, no. 1 (2014): 73-79. https://doi.org/10.3892/etm.2013.1353
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