Compared with the cells on TCPS, BMSCs cultured on decellularized ECm showed a spindle-like shape, a robust proliferative capacity and suppressed level of intracellular ROS, accompanied with up-regulation of superoxide dismutase genes. In contrast to hepatocyte-like cells differentiated from BMSCs on TCPS, those on decellularized

ECM were determined with a more intensive staining of glycogen storage, the urea concentration of differentiated BMSCs of ECM group was 8.7% higher than that of TCPS group at 21(10.5 ± 0.2 μg/mL/24h vs.9.7 ± 0.1 μg/mL/24h, p < 0.05) and 7.3% higher on Day 28 (10.9 ± 0.2 μg/mL/24h vs.10.2 ± 0.2μg/mL/24h, p< 0.05) and higher expressions of hepatocytespecific genes Erastin clinical trial including albumin, PD0325901 cost tryptophan 2, 3-dioxygenase, cytochrome P450 7A1, cytochrome P45。3A4, cytokeratin 18 and hepatocyte nuclear factor 4 alpha on day 7,14,21 and 28 (p < 0.05). Conclusions: Decellularized ECM deposited by BMSCs can be an effective method to facilitate in vitro expansion and hepatic maturation of BMSCs and promote developments in stem cell-based liver regenerative medicine. Disclosures: The following people have nothing to disclose: Hongliang He, Liang Peng, Yujie Su, Qiyi Zhao, Ke Wang,

Zhiliang Gao [Aim] The appearance and proliferation of liver progenitor cells (LPCs) are considered to be important steps necessary for liver regeneration. Previously, we have demonstrated the differentiation of LPCs into hepatocytes during co-culture with bone marrow cells. Moreover, FGF2 was found to be a critical factor for migration of LPCs. Using DNA microarray analysis, we identified epiregulin, a growth factor belonging to the EGF family, as a candidate growth factor acting on LPCs. However, the relationship between epiregulin

and LPCs is still unclear. The aim of the present study was to clarify the role of epiregulin during liver regeneration. [Methods] A liver injury model was developed using C57BL/6 mice fed a diet containing 0.1% 3.5diethoxycarbonyI-1.4-dihydrocoIIidine (DDC) to induce Acesulfame Potassium LPCs. We evaluated the expression of epiregulin in this DDC mouse model using immunohistochemistry (IHC) and RT-gPCR. Serum epiregulin levels were also examined in both DDC mice and patients with acute liver failure. The proliferation of an EpCAMpositive LPC cell line cultured with recombinant epiregulin was examined in vitro. Finally, overexpression of epiregulin was induced in mice by the hydrodynamic tail vein injection (HTVi) method to evaluate its effects in vivo. The expression of epiregulin, PCNA and CK19 in the mouse liver was investigated by IHC. [Results] In patients with acute liver failure, serum epiregulin levels were significantly increased in comparison with the healthy controls.