An atlas of the human liver diurnal transcriptome and its perturbation by hepatitis C virus infection.
Atish MukherjiFrank JühlingYogy SimanjuntakEmilie CrouchetFabio Del ZompoYuji TeraokaAlexandre HallerPhilippe BaltzingerSoumith ParitalaFahmida RashaNaoto FujiwaraCloé GadenneNevena SlovicMarine A OudotSarah C DurandClara PonsollesCatherine SchusterXiaodong ZhuangJacinta HolmesMing-Lun YehHiromi Abe-ChayamaMathias F HeikenwälderAngelo SangiovanniMassimo IavaroneMassimo ColomboSteven K H FoungJane A McKeatingIrwin DavidsonMing-Lung YuRaymond T ChungYujin HoshidaKazuaki ChayamaJoachim LupbergerThomas F BaumertPublished in: Nature communications (2024)
Chronic liver disease and cancer are global health challenges. The role of the circadian clock as a regulator of liver physiology and disease is well established in rodents, however, the identity and epigenetic regulation of rhythmically expressed genes in human disease is less well studied. Here we unravel the rhythmic transcriptome and epigenome of human hepatocytes using male human liver chimeric mice. We identify a large number of rhythmically expressed protein coding genes in human hepatocytes of male chimeric mice, which includes key transcription factors, chromatin modifiers, and critical enzymes. We show that hepatitis C virus (HCV) infection, a major cause of liver disease and cancer, perturbs the transcriptome by altering the rhythmicity of the expression of more than 1000 genes, and affects the epigenome, leading to an activation of critical pathways mediating metabolic alterations, fibrosis, and cancer. HCV-perturbed rhythmic pathways remain dysregulated in patients with advanced liver disease. Collectively, these data support a role for virus-induced perturbation of the hepatic rhythmic transcriptome and pathways in cancer development and may provide opportunities for cancer prevention and biomarkers to predict HCC risk.
Keyphrases
- papillary thyroid
- hepatitis c virus
- genome wide
- endothelial cells
- squamous cell
- gene expression
- single cell
- transcription factor
- dna methylation
- global health
- rna seq
- human immunodeficiency virus
- stem cells
- public health
- lymph node metastasis
- dna damage
- type diabetes
- cell therapy
- high glucose
- mesenchymal stem cells
- small molecule
- high fat diet induced
- big data
- genome wide identification
- electronic health record
- antiretroviral therapy
- liver fibrosis