EPIDERMAL GROWTH-FACTOR AND INSULIN-LIKE GROWTH FACTOR-I ENHANCE KERATINOCYTE MIGRATION
EPIDERMAL GROWTH-FACTOR AND INSULIN-LIKE GROWTH FACTOR-I ENHANCE KERATINOCYTE MIGRATION
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DOI：
10.1111/1523-1747.ep12472297
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发表时间：
1993-05-01
影响因子：
6.5
通讯作者：
JENSEN, PJ
中科院分区：
文献类型：
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作者：
ANDO, Y;JENSEN, PJ
虽然它们的作用机制尚不清楚，但许多生长因子已被证明可促进皮肤伤口修复。角质形成细胞的迁移和增殖是再上皮化所必需的，并且有证据表明这些过程可能受到一种或多种促进伤口修复的生长因子的调节。使用吞噬动力学测定，它允许直接观察迁移路径作为一个金颗粒的自由区，我们研究了表皮生长因子（EGF）和胰岛素样生长因子I（IGF-I）对人角质形成细胞迁移的影响。在不存在任何其他生长因子的情况下，将EGF添加到限定培养基中诱导过夜孵育后迁移增加2.5 - 4.5倍; EGF对迁移的影响是浓度依赖性的，最大值为10至50 ng/ml EGF。IGF-I和胰岛素也同样观察到角质形成细胞迁移的浓度依赖性增强。在所有因素下，在用胶原IV或纤连蛋白包被的胶体金板上观察到迁移，但在没有基质包被的情况下未观察到迁移。为了进一步研究表皮生长因子受体参与角质形成细胞迁移，我们测试了作为拮抗剂的表皮生长因子受体的单克隆抗体的作用。EGF诱导的迁移被这种抗体完全阻止;然而，胰岛素或IGF-I的增强作用没有被阻断。这些结果表明，IGF-I和胰岛素增强角质形成细胞迁移的机制不同于EGF。
Although their mechanisms of action are unclear, a number of growth factors has been shown to promote cutaneous wound repair. Keratinocyte migration and proliferation are required for re-epithelialization, and there is evidence to suggest that these processes may be regulated by one or more growth factors that promote wound repair. Using the phagokinetic assay, which allows direct observation of migration path as a gold-particle-free area, we examined the effects of epidermal growth factor (EGF) and insulin-like growth factor I (IGF-I) on human keratinocyte migration. Addition of EGF to defined medium in the absence of any other growth factor induced an increase in migration of 2.5 - 4.5 fold after overnight incubation; the effect of EGF on migration was concentration dependent, with a maximum at 10 to 50 ng/ml EGF. Concentration-dependent enhancement of keratinocyte migration was similarly observed with IGF-I as well as insulin. With all factors, migration was observed on colloidal gold plates coated with collagen IV or with fibronectin but not in the absence of matrix coating. To examine further the involvement of the EGF receptor in keratinocyte migration, we tested the effect of a monoclonal antibody to the EGF receptor that acts as an antagonist. EGF-induced migration was completely prevented by this antibody; however, the enhancement by insulin or IGF-I was not blocked. These results suggest that IGF-I and insulin enhance keratinocyte migration by a mechanism distinct from that of EGF.