Inhibition of 125I-epidermal growth factor binding to cultured keratinocytes by antiproliferative molecules gamma interferon, cyclosporin A, and transforming growth factor-beta.
Inhibition of 125I-epidermal growth factor binding to cultured keratinocytes by antiproliferative molecules gamma interferon, cyclosporin A, and transforming growth factor-beta.
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抗增殖分子γ干扰素、环孢菌素A和转化生长因子-β抑制125I-表皮生长因子与培养的角质形成细胞的结合。
DOI：
10.1111/1523-1747.ep12284427
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Mitra,RS
中科院分区：
文献类型：
--
作者：
Nickoloff,BJ;Mitra,RS
γ-干扰素（IFN-γ）、环孢菌素A和转化生长因子β（TGF-β）对培养的人角质形成细胞（KC）的生长有抑制作用，而肿瘤坏死因子（TNF-α）对KC的生长无抑制作用。当这些抗增殖分子被加入KC中时，它们诱导了125 I-表皮生长因子（I-EGF）结合的浓度和时间依赖性抑制。这些抗增殖分子主要减少结合位点的数量约25%-50%，而不影响结合亲和力。肿瘤坏死因子不影响I-EGF与配体的结合。与抗增殖分子抑制I-EGF结合的能力平行，转化生长因子-α产生增加。这些结果表明，几种不同的抗增殖分子可能有一个共同的机制，通过减少I-EGF结合KC抑制细胞生长。
The growth of cultured human keratinocytes (KC) is inhibited by gamma interferon (IFN-γ), cyclosporin A and transforming growth factor-beta, but not by tumor necrosis facto. When these antiproliferative molecules were added to KC they induced a concentration and time-dependent inhibition of125I-epidermal growth factor (I-EGF) binding. These antiproliferative molecules primarily reduced the number of binding sites by approximately 25%-50% without affecting the binding affinity. Tumor necrosis factor did not influence the ligand binding by I-EGF. In parallel with the ability of the antiproliferative molecules to inhibit I-EGF binding, there was an increase in transforming growth factor-alpha production. These results suggest that several different antiproliferative molecules may share a common mechanism to inhibit cell growth by reducing I-EGF binding to KC.