944 THERAPEUTIC POTENTIAL OF HUMAN PLACENTA-DERIVED STEM CELLS IN THE CCL4-INJURED RATS DEPENDS ON TRANSPLANTATION ROUTES

POSTERSrespectively.Cell survival was assayed by cytotoxicity assays and the expression of c-Jun and its potential target genes was analyzed.Results: Chemical induction of ER stress resulted in a rapid and robust expression of c-Jun in both, human hepatoma cells and mouse primary hepatocytes, but surprisingly, no major differences in ER stress-mediated cell death were observed in cells lacking c-Jun.However, massive cytoplasmic vacuolization occurred upon ER stress in primary knock-out hepatocytes, most likely due to expansion of the ER.A similar phenotype was observed in primary hepatocytes in which Jun N-terminal kinases, important regulators of c-Jun activity, were inhibited pharmacologically.This vacuolization correlated with increased expression of ER stress marker genes such as gadd153, bip and spliced xbp-1 and subsequent expression of several chemokines including CXCL1 and CXCL2.Recent findings suggest that ER expansion is tightly controlled by self-degradation of these organelles in a process called autophagy.Interestingly, autophagy appeared to be impaired in the absence of c-Jun.Conclusions: These findings suggest that c-Jun, although not essential for hepatocyte survival, tightly controls the hepatocellular response to ER stress possibly by interacting with the autophagy machinery.