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首页> 外文期刊>Journal of Cellular Physiology >Expression of insulin-like growth factor binding protein-3 (IGFBP-3) in human keratinocytes is regulated by EGF and TGFbeta1.
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Expression of insulin-like growth factor binding protein-3 (IGFBP-3) in human keratinocytes is regulated by EGF and TGFbeta1.

机译：胰岛素样生长因子的表达绑定在人类角质细胞蛋白质3 (IGFBP-3)受EGF和TGFbeta1。

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Insulin-like growth factor-I (IGF-I) is essential for normal epidermal homeostasis; however, the role of IGF binding proteins (IGFBPs), regulators of IGF action, remains unclear. Here we examine the regulation of human keratinocyte-produced IGFBPs by epidermal growth factor (EGF), transforming growth factor beta 1 (TGFbeta1), and IGF-I, growth factors known to be active in skin. In the absence of added growth factors, IGFBP-3 was the major binding protein secreted into the medium by primary keratinocytes. Addition of EGF or TGFbeta1 to keratinocyte cultures resulted in a significant decrease in IGFBP-3 abundance in conditioned medium when compared with control, untreated cells. Specifically, EGF (50 ng/ml) and TGFbeta1 (50 ng/ml) reduced IGFBP-3 abundance to 15+/-6% and 22+/-9%, respectively. Using Northern blot analysis, we found EGF and TGFbeta1 (50 ng/ml) to reduce IGFBP-3 mRNA levels in keratinocytes to 51+/-12% and 50+/-38%, respectively, when compared with control, untreated cells. Treatment with IGF-I or its analogue des(1-3)IGF-I did not lead to any consistent change in IGFBP-3 abundance. However, both IGF-I and des(1-3)IGF-I at 100 ng/ml led to a modest increase in IGFBP-3 mRNA levels in keratinocytes, suggesting posttranscriptional regulation of IGFBP-3 abundance. We propose that local modulation of IGFBP-3 abundance may represent another level of regulation of growth factor action in the epidermis, where EGF and TGFbeta1 and possibly other local growth factors specifically regulate the availability of IGF-I to its keratinocyte receptors.
机译：胰岛素样生长因子(IGF-I)是至关重要的正常表皮内稳态;胰岛素样生长因子结合蛋白研究的角色(IGFBPs),监管机构IGF的行动,还不清楚。人类keratinocyte-produced的规定IGFBPs表皮生长因子(EGF),转化生长因子β1 (TGFbeta1),IGF-I,生长因子被认为是活跃于皮肤。在没有添加生长因子,IGFBP-3主要结合蛋白分泌到媒介通过主要的角质细胞。或TGFbeta1角化细胞文化导致IGFBP-3丰度明显下降条件培养基与控制相比,未经处理的细胞。TGFbeta1 (50 ng / ml)减少IGFBP-3丰富15 + / - -6%和22 + / - -9%,分别。污点分析,我们发现EGF和TGFbeta1 (50ng / ml)减少IGFBP-3 mRNA水平角化细胞51 + / - -12%和50 + / - -38%,分别与控制相比,未经处理的细胞。模拟des IGF-I没有导致任何(1 - 3)IGFBP-3丰度的变化一致。IGF-I和des (1 - 3) IGF-I 100 ng / ml导致适度增加IGFBP-3 mRNA水平角化细胞,这表明转录后的监管IGFBP-3丰富。当地的调制IGFBP-3丰富代表增长的另一个层面的监管因素作用的表皮,表皮生长因子和TGFbeta1甚至其他地方生长因子具体调节IGF-I的可用性角化细胞受体。

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