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首页> 外文期刊>American Journal of Physiology >New primary culture systems to study the differentiation and proliferation of mouse fetal hepatoblasts
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New primary culture systems to study the differentiation and proliferation of mouse fetal hepatoblasts

机译：研究小鼠胎儿成肝细胞分化和增殖的新的原代培养系统

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First published December 20, 2007; doi:10.1152/ajpgi.00412.2007.-Hepatoblasts have the potential to differentiate into both hepatocytes and biliary epithelial cells through a differentiation program that has not been fully elucidated. With the aim to better define the mechanism of differentiation of hepatoblasts, we isolated hepatoblasts and established new culture systems. We isolated hepatoblasts from E12.5 fetal mouse liver by using E-cadherin. The E-cadherin+ cells expressed alpha-fetoprotein (AFP) and albumin (Alb) but not cytokeratin 19 (CK19). Transplantation of the E-cadherin+ cells into mice that had been subjected to liver injury or biliary epithelial injury led to differentiation of the cells into hepatocytes or biliary epithelial cells, respectively. In a low-cell-density culture system in the absence of additional growth factors, E-cad-herin+ cells formed colonies of various sizes, largely comprising Alb-positive cells. Supplementation of the culture medium with he-patocyte growth factor and epidermal growth factor promoted proliferation of the cells. Thus the low-cell-density culture system should be useful to identify inductive factors that regulate the proliferation and differentiation of hepatoblasts. In a high-cell-density system in the presence of oncostatin M+dexamethasone, E14.5, but not E12.5, E-cadherin+ cells differentiated into mature hepatocytes, suggesting that unidentified factors are involved in hepatic maturation. Culture of E-cadherin+ cells derived from E12.5 or E14.5 liver under high-cell-density conditions should allow elucidation of the mechanism of hepatic differentiation in greater detail. These new culture systems should be of use to identify growth factors that induce hepatoblasts to proliferate or differentiate into hepatocytes and biliary epithelial cells.
机译：首次发布于2007年12月20日; doi：10.1152 / ajpgi.00412.2007.-成肝细胞有可能通过尚未完全阐明的分化程序分化为肝细胞和胆管上皮细胞。为了更好地定义成肝细胞的分化机制，我们分离了成肝细胞并建立了新的培养系统。我们使用E-钙粘着蛋白从E12.5胎鼠肝脏分离了成肝细胞。 E-钙粘着蛋白+细胞表达甲胎蛋白（AFP）和白蛋白（Alb），但不表达细胞角蛋白19（CK19）。将E-钙粘蛋白+细胞移植到已经遭受肝损伤或胆道上皮损伤的小鼠中，导致细胞分别分化为肝细胞或胆道上皮细胞。在没有其他生长因子的低细胞密度培养系统中，E-cad-herin +细胞形成各种大小的菌落，主要包含Alb阳性细胞。补充肝细胞生长因子和表皮生长因子的培养基促进了细胞的增殖。因此，低细胞密度培养系统应可用于鉴定调节成肝细胞增殖和分化的诱导因子。在存在抑瘤素M +地塞米松（E14.5）而非E12.5的高细胞密度系统中，E-钙粘着蛋白+细胞分化为成熟的肝细胞，这表明未知的因素参与了肝的成熟。在高细胞密度条件下培养源自E12.5或E14.5肝脏的E-cadherin +细胞应能更详细地阐明肝脏分化的机制。这些新的培养系统应用于鉴定诱导成肝细胞增殖或分化为肝细胞和胆管上皮细胞的生长因子。

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