Yoneda T, Pratt R M
Differentiation. 1981;19(3):194-8. doi: 10.1111/j.1432-0436.1981.tb01147.x.
Previous studies of ours have shown that palatal mesenchymal cells from the human embryo (HEPM cells) are responsive both to the glucocorticoid dexamethasone (DEX) and epidermal growth factor (EGF) through mechanisms associated with cytoplasmic and cell surface receptors, respectively. HEPM cell growth was inhibited by DEX and was stimulated by EGF. In the present study, the interactions between DEX and EGF were investigated. DEX (10(-6) M) enhanced EGF-stimulated HEPM cell growth as assessed by an increase in cell number and ornithine decarboxylase activity under serum-free cell culture conditions. DEX also enhanced the specific binding of 125I-EGF to these cells, which was reflected in an increase in both the number and the affinity of EGF receptors. EGF (1 ng/ml), on the other hand, decreased the number of sites per cell which specifically bind 3H-DEX. EGF completely prevented the inhibition by DEX of HEPM cell growth. These results indicated that DEX and EGF interact with each other in the process(es) regulating HEPM cell growth. This interaction may be partially influenced by direct modulation of existing receptors for DEX and EGF present in the cells.
我们之前的研究表明,来自人类胚胎的腭间充质细胞(HEPM细胞)分别通过与细胞质受体和细胞表面受体相关的机制,对糖皮质激素地塞米松(DEX)和表皮生长因子(EGF)产生反应。DEX抑制HEPM细胞生长,而EGF刺激其生长。在本研究中,对DEX和EGF之间的相互作用进行了研究。在无血清细胞培养条件下,通过细胞数量增加和鸟氨酸脱羧酶活性评估,DEX(10⁻⁶ M)增强了EGF刺激的HEPM细胞生长。DEX还增强了¹²⁵I-EGF与这些细胞的特异性结合,这表现为EGF受体数量和亲和力的增加。另一方面,EGF(1 ng/ml)减少了每个细胞特异性结合³H-DEX的位点数量。EGF完全阻止了DEX对HEPM细胞生长的抑制。这些结果表明,DEX和EGF在调节HEPM细胞生长的过程中相互作用。这种相互作用可能部分受到对细胞中现有DEX和EGF受体的直接调节的影响。