Bulk liver mRNA-seq of Cep72 knockout and wild-type mice in Schistosoma japonicum infection–induced and CCl4-induced liver fibrosis models

Liver fibrosis is a common pathological outcome of chronic liver injury triggered by diverse etiologies. To investigate the role of CEP72 in fibrogenesis under distinct fibrotic settings, we performed bulk mRNA sequencing of whole-liver total RNA from wild-type (WT) and Cep72 knockout (Cep72-KO) mice in two experimental models: Schistosoma japonicum (Sj) infection–induced liver fibrosis and carbon tetrachloride (CCl4)–induced liver fibrosis. For the Sj model, mice were percutaneously infected with 17 ± 1 Schistosoma japonicum cercariae per mouse and analyzed at 8 weeks post infection, generating four groups: 8W-NC (WT control), 8W-KO-NC (Cep72-KO control), 8W-Sj (WT + Sj infection), and 8W-Sj-KO (Cep72-KO + Sj infection) (n = 2 mice per group). For the CCl4 model, mice were treated for 8 weeks with intraperitoneal injections of 10% CCl4 at 10 μL/g body weight, twice per week, and samples were collected from 8W-CCL4 (WT + CCl4) and 8W-KO-CCL4 (Cep72-KO + CCl4) groups (n = 2 mice per group). Paired-end Illumina mRNA-seq was performed on extracted total RNA from whole liver tissue. This dataset enables comparative transcriptomic analyses to identify CEP72-associated gene expression programs and pathways involved in liver injury, inflammation, and fibrosis across parasitic and chemical models.