CCL1 and cholestasis: These changes were accompanied by a reduced inflammatory response as determined by F4/80 and Il-6, Ccl1 and iNos expression, as well as less fibrosis evaluated through Sirius red staining and the levels of profibrogenic (Tgfb, Timp1, and Timp2) genes (Fig. 5f and Suppl Fig. 6b). Altogether, these data suggest that anti-miR-873-5p targeting in the Mdr2-/-cholestasis animal model reduces cholangiocyte proliferation, increases the export of bile acids and ameliorates BA-induced hepatocyte cell death and inflammatory response.