GSE110404
Bone morphogenetic protein 8b (bmp8b) in non-alcoholic steatohepatitis (nash), acute hepatic damage and liver regeneration
TGFß/BMP family member Bone Morphogenetic Protein 8b (Bmp8b) is upregulated in NASH (Western Diet -WD- Model), acute liver damage (CCl4 model) and by Partial Hepatectomy (PH). Absence of Bmp8b reduces liver inflammation and fibrosis in the NASH model (WD). In the acute (3days) CCl4 model, absence of Bmp8b impacts acute inflammatory responses, hepatic stellate cells (HSC) activation, and compensatory hepatocyte proliferation; defective inflammatory pathways and hepatocytes proliferation is also observed in the Partial hepatectomy model. BMP8b is thus a pathophysiologically relevant target to modulate the responses to damage in acute and chronic liver disease. Overall design: Male C57BL/6J mice (WT littermates and/or Bmp8b KO mice - WD experiment: 9 weeks old; CCl4 & PH: 16 weeks old) were challenged with: A) Western (Teklad, TD88137) or Low Fat Control (Teklad, TD08485) Diet for 32 weeks; B) IP injection of 2ul/g body weight of olive Oil (OO) or CCl4:olive oil [1:1 (v/v)] mix; Mice were culled 3 days after IP injection; or C) Partial Hepatectomy; Mice were culled 3 days after surgery.