This study investigates the role of group VIA calcium-independent phospholipase A2 (iPLA2β) in non-alcoholic steatohepatitis (NASH) using myeloid- and hepatocyte-specific Knockout mouse models. The researchers found that deletion of iPLA2β in myeloid cells exacerbated liver inflammation and fibrosis, while its deletion in hepatocytes attenuated these effects during methionine-choline-deficient (MCD) diet-induced NASH. These findings highlight the cell-type-specific functions of iPLA2β in NASH pathogenesis.
iPLA2β plays divergent roles in NASH depending on the cell type: its deletion in myeloid cells worsens liver pathology, while its deletion in hepatocytes has protective effects. This suggests that therapeutic strategies targeting iPLA2β should consider its cell-specific functions.
Myeloid-specific iPLA2β Knockout mice and hepatocyte-specific iPLA2β Knockout mice, generated using Cre-loxP technology with LysM-Cre and Albumin-Cre drivers, respectively.
Non-alcoholic steatohepatitis (NASH), Liver inflammation, Fibrosis, Phospholipase A2, Cell-type-specific gene function
Conditional Knockout models, Cre-loxP system, LysM-Cre, Albumin-Cre, MCD diet-induced NASH
From model design to experimental results
Tailor-made solutions adapted to scientific questions
Comprehensive dataset package
Generated with biopharma partners and in-house
Scientific follow-up and advice along the project
Collaborative approach for problem solving and development of innovative models
Breeding facilities in US and Europe
Certified health status from professional breeders
