Moore Rebecca N, Dasgupta Anouska, Rajaei Nayyereh, Yarmush Martin L, Toner Mehmet, Larue Lionel, Moghe Prabhas V
Department of Biomedical Engineering, Rutgers University, Piscataway, New Jersey, USA.
Biotechnol Bioeng. 2008 Dec 15;101(6):1332-43. doi: 10.1002/bit.21987.
We examined the effects of co-cultivated hepatocytes on the hepatospecific differentiation of murine embryonic stem (ES) cells. Utilizing an established mouse ES cell line expressing high or low levels of E-cadherin, that we have previously shown to be responsive to hepatotrophic growth factor stimulation (Dasgupta et al., 2005. Biotechnol Bioeng 92(3):257-266), we compared co-cultures of cadherin-expressing ES (CE-ES) cells with cultured rat hepatocytes, allowing for either paracrine interactions (indirect co-cultures) or both juxtacrine and paracrine interactions (direct co-cultures, random and patterned). Hepatospecific differentiation of ES cells was evaluated in terms of hepatic-like cuboidal morphology, heightened gene expression of late maturation marker, glucose-6-phosphatase in relation to early marker, alpha-fetoprotein (AFP), and the intracellular localization of albumin. Hepatocytes co-cultured with growth factor primed CE-ES cells markedly enhanced ES cell differentiation toward the hepatic lineage, an effect that was reversed through E-cadherin blockage and inhibited in control ES cells with reduced cadherin expression. Comparison of single ES cell cultures versus co-cultures show that direct contact co-cultures of hepatocytes and CE-ES cells maximally promoted ES cell commitment towards hepatodifferentiation, suggesting cooperative effects of cadherin-based juxtacrine and paracrine interactions. In contrast, E-cadherin deficient mouse ES (CD-ES) cells co-cultured with hepatocytes failed to show increased G6P expression, confirming the role of E-cadherin expression. To establish whether albumin expression in CE-ES cells was spatially regulated by co-cultured hepatocytes, we co-cultivated CE-ES cells around micropatterned, pre-differentiated rat hepatocytes. Albumin localization was enhanced "globally" within CE-ES cell colonies and was inhibited through E-cadherin antibody blockage in all but an interfacial band of ES cells. Thus, stem cell based cadherin presentation may be an effective tool to induce hepatotrophic differentiation by leveraging both distal/paracrine and contact/juxtacrine interactions with primary cells of the liver.
我们研究了共培养的肝细胞对小鼠胚胎干细胞(ES细胞)肝特异性分化的影响。利用我们先前已证明对肝细胞生长因子刺激有反应的、表达高水平或低水平E-钙黏蛋白的既定小鼠ES细胞系(Dasgupta等人,2005年。《生物技术与生物工程》92(3):257 - 266),我们比较了表达钙黏蛋白的ES(CE-ES)细胞与培养的大鼠肝细胞的共培养情况,包括旁分泌相互作用(间接共培养)或旁分泌和近分泌相互作用(直接共培养,随机和模式化)。ES细胞的肝特异性分化通过类肝立方形态、晚期成熟标志物葡萄糖-6-磷酸酶相对于早期标志物甲胎蛋白(AFP)的基因表达升高以及白蛋白的细胞内定位来评估。与生长因子预处理的CE-ES细胞共培养的肝细胞显著增强了ES细胞向肝谱系的分化,这种效应通过E-钙黏蛋白阻断而逆转,并在钙黏蛋白表达降低的对照ES细胞中受到抑制。单一ES细胞培养与共培养的比较表明,肝细胞与CE-ES细胞的直接接触共培养最大程度地促进了ES细胞向肝分化的定向分化,表明基于钙黏蛋白的近分泌和旁分泌相互作用具有协同效应。相反,与肝细胞共培养的E-钙黏蛋白缺陷型小鼠ES(CD-ES)细胞未能显示G6P表达增加,证实了E-钙黏蛋白表达的作用。为了确定CE-ES细胞中白蛋白的表达是否受共培养的肝细胞空间调控,我们在微模式化、预分化的大鼠肝细胞周围共培养CE-ES细胞。白蛋白定位在CE-ES细胞集落内“整体”增强,并在除ES细胞界面带外的所有区域通过E-钙黏蛋白抗体阻断而受到抑制。因此,基于干细胞的钙黏蛋白呈现可能是一种通过利用与肝脏原代细胞的远端/旁分泌和接触/近分泌相互作用来诱导肝营养分化的有效工具。