Non cell autonomous upregulation of CDKN2 transcription linked to progression of chronic hepatitis C disease.
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.
MRC - University of Glasgow Centre for Virus Research, Glasgow, UK.
Mark W
MW
Robinson
Dagmara
D
McGuinness
Rachael
R
Swann
Stephen
S
Barclay
Peter R
PR
Mills
Arvind H
AH
Patel
John
J
McLauchlan
Paul G
PG
Shiels
D016022:Case-Control Studies; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000235:genetics*; D018450:Disease Progression; D056426:Genetic Loci; D019698:Hepatitis C, Chronic / Q000235:genetics* / Q000473:pathology*; D006801:Humans; D008103:Liver Cirrhosis / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D059505:Telomere Homeostasis / Q000235:genetics; D014158:Transcription, Genetic; D015854:Up-Regulation / Q000235:genetics*
D019941:Cyclin-Dependent Kinase Inhibitor p16; D012333:RNA, Messenger
CDKN2 locus; biological aging; chronic HCV infection; telomere length