Insulin-like growth factors, insulin, and epidermal growth factor cause rapid cytoskeletal reorganization in KB cells. Clarification of the roles of type I insulin-like growth factor receptors and insulin receptors.
Insulin-like growth factors, insulin, and epidermal growth factor cause rapid cytoskeletal reorganization in KB cells. Clarification of the roles of type I insulin-like growth factor receptors and insulin receptors.
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胰岛素样生长因子、胰岛素和表皮生长因子导致 KB 细胞快速细胞骨架重组。
DOI：
10.1016/s0021-9258(18)66689-x
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
M. Kasuga
中科院分区：
文献类型：
--
作者：
T. Kadowaki;S. Koyasu;E. Nishida;H. Sakai;F. Takaku;I. Yahara;M. Kasuga
胰岛素样生长因子（IGF） I（大于或等于10(-10)M）、胰岛素样生长因子II（大于或等于10(-9)M）、胰岛素（大于或等于10(-9)M）和表皮生长因子（EGF，大于或等于10(-11)M）引起KB细胞快速的膜褶皱。在加入这些生长因子后1 min内观察到形态变化，并伴有微丝重组，而不伴有微管重组。IGF-I、IGF-II和胰岛素诱导的膜皱褶在形态上非常相似或相同，IGF-I大于IGF-II大于胰岛素，而egf诱导的膜皱褶在形态上不同。KB细胞具有EGF受体、I型IGF受体和胰岛素受体，但II型IGF受体很少或不存在。针对I型IGF受体的单克隆抗体，完全抑制125I-IGF-I与细胞的结合，但不抑制125i -胰岛素的结合，引起IGF-I （10(-8) M）刺激的膜褶皱明显抑制。在该抗体的存在下，IGF-II （10(-8) M）刺激的膜起皱被部分抑制，而胰岛素（10(-7)M）刺激的膜起皱仅被轻微抑制。相反，抗胰岛素受体单克隆抗体可阻断胰岛素（10(-7)M）刺激，但不能阻断IGF-I （10(-8) M）刺激。因此，本研究提供的证据表明，IGF-I和胰岛素主要通过它们自己的（同源）受体起作用，而IGF- ii通过与I型IGF和胰岛素（异源）受体交叉反应，引起细胞骨架结构的快速改变。
Insulin-like growth factor (IGF) I (greater than or equal to 10(-10)M, insulin-like growth factor II (greater than or equal to 10(-9) M), insulin (greater than or equal to 10(-9) M, and epidermal growth factor (EGF, greater than or equal to 10(-11) M) caused rapid membrane ruffling in KB cells. The morphological change was observed within 1 min after the addition of these growth factors and was accompanied by microfilament reorganization, but not by microtubule reorganization. IGF-I, IGF-II, and insulin induced morphologically very similar or identical membrane ruffles with the order of potency IGF-I greater than IGF-II greater than insulin, whereas EGF-induced membrane ruffles were morphologically different. KB cells possessed EGF receptors, type I IGF receptors, and insulin receptors, but few or no type II IGF receptors. Monoclonal antibody against type I IGF receptors, which completely inhibited the binding of 125I-IGF-I to the cells but did not inhibit the binding of 125I-insulin, caused marked inhibition of IGF-I (10(-8) M)-stimulated membrane ruffling. IGF-II (10(-8) M)-stimulated membrane ruffling was partially inhibited in the presence of this antibody, but insulin (10(-7) M)-stimulated membrane ruffling was only slightly inhibited. In contrast, monoclonal antibody against insulin receptors blocked insulin (10(-7) M) stimulation, but not IGF-I (10(-8) M) stimulation, of membrane ruffling. Thus, this study provides evidence that IGF-I and insulin act mostly through their own (homologous) receptors and that IGF-II acts by cross-reacting with both type I IGF and insulin (heterologous) receptors in causing rapid alterations in cytoskeletal structure.