Modulation of cell competence for induction of differentiation in myeloid leukemic cells
Modulation of cell competence for induction of differentiation in myeloid leukemic cells
复制标题
调节细胞能力以诱导骨髓白血病细胞分化
DOI：
10.1002/jcp.1041110103
复制
发表时间：
1982
影响因子：
5.6
通讯作者：
L. Sachs
中科院分区：
文献类型：
--
作者：
G. Symonds;L. Sachs
研究表明，小鼠髓性白血病细胞的分化缺陷克隆（MGI−D−克隆）被诱导产生某些分化相关特性的能力是可以调节的。对于某些诱导剂，这是通过改变血清类型来实现的，对于另一种诱导剂，通过从培养基中去除血清来实现。在无血清培养基或含马、小牛、兔或绵羊血清的培养基中，不能通过正常巨噬细胞和粒细胞诱导蛋白MGI（MGI-2）、脂多糖（LPS）或地塞米松（Dex）的分化诱导形式诱导分化的所有克隆（非允许血清）可以被所有三种诱导剂诱导，在同基因或同种异体小鼠血清或大鼠血清（许可血清）中溶菌酶和Fc和/或C3受体的分化相关性质。仅通过洗涤细胞和改变血清类型就改变了诱导分化的能力，并且加入非允许血清阻断了允许血清的诱导。这种增加的能力与伴刀豆球蛋白A形成帽的能力增加有关。去除血清后，一些MGI−D−克隆被胰岛素诱导产生溶菌酶、Fc和C3受体。然而，血清类型的变化和血清的去除都不能调节这些克隆中肿瘤促进剂12-O-十四烷酰基佛波醇-13-乙酸酯的诱导作用。与MGI−D−克隆相反，改变血清类型或去除血清不会调节MGI-2、LPS、Dex或胰岛素在其他髓性白血病细胞克隆中的诱导作用，这些细胞克隆可以在马或小牛血清中被MGI-2诱导部分分化（MGI+D−克隆）或完全分化（MGI+D+克隆）。结果表明，通过适当的调节，所有测试的MGI−D−克隆都可以被诱导产生一些分化相关特性;在允许的血清中存在允许MGI−D−克隆被MGI-2、LPS和Dex诱导的因子;在非允许的血清中存在阻断这种诱导的其他因子;并且在无血清培养基中，适当克隆的细胞可以变得对胰岛素诱导的这些特性敏感。
It is shown that the competence of differentiation‐defective clones of mouse myeloid leukemic cells (MGI−D− clones) to be induced for some differentiation‐associated properties can be modulated. For certain inducers this was effected by changing the type of serum and for another inducer by removing serum from the culture medium. All the clones which could not be induced to differentiate by the differentiation‐inducing from of the normal macrophage and granulocyte inducing proteins MGI (MGI‐2), lipopolysaccharide (LPS), or dexamethasone (Dex) in serum‐free medium or in medium with horse, calf, rabbit, or sheep serum (nonpermissive serum) could be induced, by all three inducers, for the differentiation‐associated properties of lysozyme and Fc and/or C3 rosettes in syngeneic or allogeneic mouse serum or rat serum (permissive serum). The competence for induction of differentiation was altered merely by washing the cells and changing the type of serum, and addition of nonpermissive serum blocked the induction in permissive serum. This increased competence was associated with an increase in the ability for cap formation by concanavalin A. Removal of serum allowed some MGI−D− clones to be induced for lysozyme, Fc, and C3 rosettes by insulin. However, neither the changes in type of serum nor the removal of serum modulated in these clones the inducing effect of the tumor promoter 12‐O‐tetradecanoylphorbol‐13‐acetate. In contrast to the MGI−D− clones, changing the serum type or removing the serum did not modulate inducibility by MGI‐2, LPS, Dex, or insulin in other clones of myeloid leukemic cells that could be induced by MGI‐2 to differentiate either partly (MGI+D− clones) or completely (MGI+D+ clones) in horse or calf serum. The results indicate that by the appropriate modulation all MGI−D− clones tested could be induced for some differentiation‐associated properties; that there are factor(s) present in permissive sera which allow MGI−D− clones to be induced by MGI‐2, LPS, and Dex; that there are other factor(s) in nonpermissive sera which block this induction; and that in serum‐free medium cells of the appropriate clone can become susceptible to induction of these properties by insulin.