Mutual Antagonism between Circadian Protein Period 2 and Hepatitis C Virus Replication in Hepatocytes

Gastroenterology Unit, IRCCS "Casa Sollievo della Sofferenza", Hospital San Giovanni Rotondo (FG), San Giovanni, Italy.
PLoS ONE (Impact Factor: 3.23). 04/2013; 8(4):e60527. DOI: 10.1371/journal.pone.0060527
Source: PubMed


Hepatitis C virus (HCV) infects approximately 3% of the world population and is the leading cause of liver disease, impacting hepatocyte metabolism, depending on virus genotype. Hepatic metabolic functions show rhythmic fluctuations with 24-h periodicity (circadian), driven by molecular clockworks ticking through translational-transcriptional feedback loops, operated by a set of genes, called clock genes, encoding circadian proteins. Disruption of biologic clocks is implicated in a variety of disorders including fatty liver disease, obesity and diabetes. The relation between HCV replication and the circadian clock is unknown.

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Available from: Manlio Vinciguerra
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    • "BxPC-3 and PANC-1 cells were cultured in DMEM supplemented with 10% fetal bovine serum (FBS), 100 U/ml penicillin and 100 ng/ml streptomycin (Invitrogen Life Technologies, Milan, Italy) while CFPAC-1 and MIA-PaCa-2 were maintained in Gibco Õ RPMI 1640 medium (Invitrogen Life Technologies, Milan, Italy) all maintained at 37 C in 5% CO 2 atmosphere incubator. Cell lines were serum shocked with 50% FBS (serum-rich medium) for 2 h in order to achieve cellular synchronization as previously described (Benegiamo et al., 2013; Pazienza et al., 2012). After 2 h, the medium used for serum shock was replaced either with normal medium supplemented with 10% FBS or with medium without FBS, and the cells were harvested at the indicated time points over 28 h. "
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