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转化生长因子β在人表皮角质形成细胞成熟中的作用。

Role of transforming growth factor beta in the maturation of human epidermal keratinocytes.

作者信息

Mansbridge J N, Hanawalt P C

机构信息

Psoriasis Research Institute, Stanford, California 94309.

出版信息

J Invest Dermatol. 1988 Mar;90(3):336-41. doi: 10.1111/1523-1747.ep12456286.

DOI:10.1111/1523-1747.ep12456286
PMID:2450142
Abstract

Changes in protein synthesis and phosphorylation in cultured human keratinocytes in response to TGF-beta have been examined by one and two dimensional electrophoresis. Transforming growth factor beta has been shown to cause little change in the rate of methionine incorporation in the concentration range in which growth is reversibly arrested. It does, however, prevent the labeling of certain specific bands detected on gels of triton-soluble proteins after 3 days of treatment. Phosphorylation of triton-soluble proteins is inhibited at concentrations of TGF-beta rather higher than the Kd of its receptor and may represent a nonphysiological effect. Nonetheless, the phosphorylation of certain prominent species is reduced. In keratinocytes cultured in delipidated serum, which show some expression of keratin 1 (67 kd) characteristic of normal maturation, TGF-beta reduces the incorporation of methionine into this keratin 1 and increases labeling of keratins 6 and 16. Transforming growth factor beta thus promotes regenerative maturation, which is normally expressed during wound healing. The ability of TGF-beta to arrest keratinocyte growth in a reversible manner and to stimulate regenerative maturation, supports its physiological role in controlling the balance between cell division, migration and maturation during epidermal wound healing.

摘要

通过一维和二维电泳研究了培养的人角质形成细胞中蛋白质合成和磷酸化对转化生长因子-β(TGF-β)的响应。已表明,在生长可逆性停滞的浓度范围内,转化生长因子-β对蛋氨酸掺入率的影响很小。然而,在处理3天后,它确实会阻止在Triton可溶蛋白凝胶上检测到的某些特定条带的标记。在高于其受体解离常数(Kd)的TGF-β浓度下,Triton可溶蛋白的磷酸化受到抑制,这可能代表一种非生理效应。尽管如此,某些突出条带的磷酸化仍会减少。在缺乏脂质的血清中培养的角质形成细胞显示出一些正常成熟特征的角蛋白1(67 kd)的表达,TGF-β减少了蛋氨酸掺入这种角蛋白1的量,并增加了角蛋白6和16的标记。因此,转化生长因子-β促进再生成熟,这在伤口愈合过程中通常会表达。TGF-β以可逆方式阻止角质形成细胞生长并刺激再生成熟的能力,支持了其在控制表皮伤口愈合过程中细胞分裂、迁移和成熟之间平衡的生理作用。

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