Non cell autonomous upregulation of CDKN2 transcription linked to progression of chronic hepatitis C disease

Aging Cell. 2013 Dec;12(6):1141-3. doi: 10.1111/acel.12125. Epub 2013 Aug 12.

Abstract

Chronic hepatitis C virus infection (C-HC) is associated with higher mortality arising from hepatic and extrahepatic disease. This may be due to accelerated biological aging; however, studies in C-HC have thus far been based solely on telomere length as a biomarker of aging (BoA). In this study, we have evaluated CDKN2 locus transcripts as alternative BoAs in C-HC. Our results suggest that C-HC induces non-cell-autonomous senescence and accelerates biological aging. The CDKN2 locus may provide a link between C-HC and increased susceptibility to age-associated diseases and provides novel biomarkers for assessing its impact on aging processes in man.

Keywords: CDKN2 locus; biological aging; chronic HCV infection; telomere length.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Case-Control Studies
  • Cyclin-Dependent Kinase Inhibitor p16 / genetics*
  • Disease Progression*
  • Genetic Loci
  • Hepatitis C, Chronic / genetics*
  • Hepatitis C, Chronic / pathology*
  • Humans
  • Liver Cirrhosis / genetics
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Telomere Homeostasis / genetics
  • Transcription, Genetic*
  • Up-Regulation / genetics*

Substances

  • Cyclin-Dependent Kinase Inhibitor p16
  • RNA, Messenger