Cell position regulates endodermal differentiation in embryonal carcinoma cell aggregates.
Cell position regulates endodermal differentiation in embryonal carcinoma cell aggregates.
复制标题
细胞位置调节胚胎癌细胞聚集体中的内胚层分化。
DOI：
10.1016/0012-1606(83)90339-1
复制
发表时间：
1983
影响因子：
2.7
通讯作者：
J. Nilsson
中科院分区：
文献类型：
--
作者：
M. Rosenstraus;J. Spadoro;J. Nilsson
有人提出，细胞位置调节小鼠胚胎内细胞团和胚胎癌细胞聚集体中的内胚层分化。该假设指出，位于细胞团和囊胚腔液体或培养基之间界面的细胞分化为内胚层，而位于内部的细胞则遵循替代的发育途径。为了测试细胞位置假说，将多能 PSA-1 细胞与次黄嘌呤磷酸核糖基转移酶缺陷的壁层样内胚层细胞聚集在一起。所得聚集体由被内胚层细胞包围的 PSA-1 细胞核心组成。使用放射自显影术来区分作为EC细胞分化产物的内胚层细胞和外源内胚层。碱性磷酸酶染色用于区分 EC 细胞和内胚层细胞。正如细胞位置假说所预测的，PSA-1 EC 细胞均位于内部，不会分化为内胚层细胞。分化的非特异性抑制并不能解释 PSA-1 衍生内胚层的缺乏，因为此类聚集体中的 PSA-1 细胞确实分化为柱状外胚层样细胞。类似的实验也用F9细胞进行。在这种情况下，聚集培养物含有视黄酸以诱导F9细胞分化为内脏内胚层。在含有被壁样内胚层细胞包围的 F9 细胞的培养物中，无论是放射自显影还是通过检测甲胎蛋白（一种内脏内胚层标记物）的产生，都没有检测到 F9 衍生的内胚层。因此，视黄酸诱导的内胚层分化也受细胞位置的调节。总的来说，上述结果为细胞位置调节 EC 细胞聚集体中内胚层分化的假设提供了有力的证据。
It has been suggested that cell position regulates endodermal differentiation in mouse embryo inner cell masses and in aggregates of embryonal carcinoma (EC) cells. This hypothesis states that cells at the interface between the cell mass and blastocoel fluid or culture medium differentiate into endoderm, whereas internally located cells follow alternative developmental pathways. To test the cell position hypothesis, pluripotent PSA-1 cells were aggregated with hypoxanthine phosphoribosyltransferase-deficient, parietal-like, endodermal cells. The resulting aggregates consisted of cores of PSA-1 cells surrounded by endodermal cells. Autoradiography was used to distinguish between endodermal cells that were the products of EC cell differentiation and the exogenous endoderm. Alkaline phosphatase staining was used to distinguish EC cells from endodermal cells. As predicted by the cell position hypothesis, the PSA-1 EC cells, all of which were internally located, did not differentiate into endodermal cells. Nonspecific inhibition of differentiation did not account for the lack of PSA-1-derived endoderm since the PSA-1 cells in such aggregates did differentiate into columnar ectodermal-like cells. Similar experiments were also conducted with F9 cells. In this case, aggregation cultures contained retinoic acid to induce F9 cells to differentiate into visceral endoderm. In cultures containing F9 cells surrounded by parietal-like endodermal cells, no F9-derived endoderm was detected either autoradiographically or by assaying for α-fetoprotein production, a visceral endoderm marker. Thus, retinoic acid-induced endodermal differentiation was also regulated by cell position. Collectively, the above results provide strong evidence for the hypothesis that cell position regulates endodermal differentiation in aggregates of EC cells.