Hepatitis C virus core or NS3/4A protein expression preconditions hepatocytes against oxidative stress and endoplasmic reticulum stress.
W Alfredo Ríos-OcampoToos DaemenManon Buist-HomanKlaas Nico FaberMaria-Cristina NavasHan MoshagePublished in: Redox report : communications in free radical research (2020)
We demonstrate that hepatocytes diminish oxidative stress through a reduction in ROS production, ER-stress markers (HSPA5 [GRP78], sXBP1) and apoptosis (caspase-3 activity) despite external oxidative stress. Interestingly, the level of the autophagy substrate protein p62 was downregulated together with HCV Core degradation, suggesting that hepatocytes can overcome excess oxidative stress through autophagic degradation of one of the stressors, thereby increasing cell survival. Duscussion: In conclusion, hepatocytes exposed to direct and indirect oxidative stress inducers are able to cope with cellular stress associated with viral hepatitis and thus promote cell survival.
Keyphrases
- oxidative stress
- endoplasmic reticulum stress
- induced apoptosis
- hepatitis c virus
- dna damage
- cell death
- ischemia reperfusion injury
- diabetic rats
- human immunodeficiency virus
- signaling pathway
- sars cov
- heat shock
- small molecule
- cell cycle arrest
- amino acid
- zika virus
- reactive oxygen species
- dengue virus
- binding protein