Study for implication of apoptotic mechanism in massive hepatic cell death and its control

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1. Acceleration of blood coagulation by apoptotic hepatocellular carcinoma HepG2 cells1) The apoptosis of Hep G2 cells was induced by staurosporin (STS).2) Phosphatidyl serine (PS) expression was detected by confocal microscopy with FITC-annexin V, a specific inhibitor of PS activity.3) The STS treatment of HepG2 cells significantly accelerated thrombin generation, which was determined using a thrombin-specific chromogenic substrate after exposing the cells to activated factor X, CaCl_2 and prothrombin. 4) The increase in thrombin generation by STS treatment was abolished following pretreatment with annexin V.These data indicate that apoptotic hepatocytes accelerate blood coagulation through the expression of a PS-dependent procoagulant surface.2. Prostaglandin receptor EP4 agonist (GPEP4A) suppression of Fas-induced apoptosis in HepG2 cells through direct Bcl-xL induction.1) GPEP4A suppressed Fas-induced apoptosis of HepG2 cells, whereas indomethacin accelerated it.2) PGE2RA significantly increased the expression levels of the Bcl-xL protein and mRNA; indomethacin decreased the expression levels, of Mdl proteins.These data indicate that direct Bcl-xL induction plays an important role in the hepatocyte protective effect induced by PGE2R-A.