Bone marrow endothelial progenitor cells activate hepatic stellate cells and aggravate carbon tetrachloride induced liver fibrosis in mice via paracrine factors.

ABSTRACT: Bone marrow derived endothelial progenitor cells (BM-EPCs) are increased in chronic liver disease (CLD). Their role in hepatic fibrosis and regeneration remains an area of intense studies. We investigated the migration and secretory functions of BM-EPCs in fibrotic mice liver. Bone marrow cells from C57BL6-GFP mice were transplanted into the femur of irradiated C57BL6 mice, followed by CCl4 doses for 8 weeks, to develop hepatic fibrosis (n = 36). Transplanted C57BL6 mice without CCl4 treatment were used as controls. EPCs were analyzed in BM, blood and liver by flow cytometry and immunofluorescence. VEGF and TGF-β were analysed in the hepatic stellate cells (HSCs) and BM-EPCs co-cultures using ELISAs. There was a significant migration of EPCs from BM to blood and to the liver (P ≤ 0.01). Pe

SUBMITTER: Garg M 

PROVIDER: S-EPMC6529081 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature