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[转录因子p53与皮肤衰老]

[Transcription factor p53 and skin aging].

作者信息

Gritsenko D A, Orlova O A, Linkova N S, Khavinson V Kh

机构信息

Institute of Plant Biology and Biotechnology, Almaty, 050040, Republic of Kazakhstan.

Saint-Petersburg Institute of Bioregulation and Gerontology, Saint-Petersburg, 197110, Russian Federation;

出版信息

Adv Gerontol. 2017;30(1):10-16.

PMID:28557384
Abstract

The review is devoted to an actual problem of cosmetics in gerontology, one of molecular aspects of skin aging. Cell renewal processes slow down with aging, and the proliferation apoptosis ratio shifts towards cell death. One of the most pivotal apoptotic markers is the transcription factor p53. p53 protein expression in the skin keratinocytes increases under the influence of ultraviolet radiation. Wherein when exposed to ultraviolet radiation mutant forms of p53 have been revealed in 70 % of keratinocytes. On the one hand, suppression of p53 expression decreases apoptosis in skin cells that slows down the process of aging. On the other hand, it promotes the development of tumors in the skin. Thus, maintaining the physiological balance of p53 expression in skin cells is important for the basic and practical cosmetic medicine in gerontology. In addition, p53 protein may be used as a functionality marker of skin cells when administered with geroprotective cosmetic means and instrumental cosmetology methods.

摘要

本综述致力于老年医学中化妆品的一个实际问题,即皮肤衰老的分子层面之一。随着年龄增长,细胞更新过程减缓,增殖凋亡比率向细胞死亡方向转变。最关键的凋亡标志物之一是转录因子p53。在紫外线辐射的影响下,皮肤角质形成细胞中的p53蛋白表达会增加。其中,在70%的角质形成细胞中发现了紫外线辐射时p53的突变形式。一方面,p53表达的抑制会减少皮肤细胞中的凋亡,从而减缓衰老过程。另一方面,它会促进皮肤肿瘤的发展。因此,维持皮肤细胞中p53表达的生理平衡对于老年医学中的基础和实用美容医学至关重要。此外,当与具有老年保护作用的美容手段和仪器美容方法一起使用时,p53蛋白可作为皮肤细胞的功能标志物。

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[Transcription factor p53 and skin aging].[转录因子p53与皮肤衰老]
Adv Gerontol. 2017;30(1):10-16.
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Resistance of senescent keratinocytes to UV-induced apoptosis.衰老角质形成细胞对紫外线诱导的细胞凋亡的抗性。
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Premature keratinocyte death and expression of marker proteins of apoptosis in human skin after UVB exposure.紫外线B照射后人皮肤中角质形成细胞过早死亡及凋亡标记蛋白的表达。
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Ultraviolet radiation triggers apoptosis of fibroblasts and skin keratinocytes mainly via the BH3-only protein Noxa.紫外线辐射主要通过仅含BH3结构域的蛋白Noxa触发成纤维细胞和皮肤角质形成细胞的凋亡。
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Gadd45a protects against UV irradiation-induced skin tumors, and promotes apoptosis and stress signaling via MAPK and p53.Gadd45a可预防紫外线照射诱导的皮肤肿瘤,并通过丝裂原活化蛋白激酶(MAPK)和p53促进细胞凋亡和应激信号传导。
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Differential p53-mediated responses to solar-simulated radiation in human papillomavirus type 16-infected keratinocytes.人乳头瘤病毒16型感染的角质形成细胞中p53介导的对太阳模拟辐射的差异反应
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Loss of Fas-ligand expression in mouse keratinocytes during UV carcinogenesis.紫外线致癌过程中小鼠角质形成细胞中Fas配体表达的丧失。
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C/EBPalpha is a DNA damage-inducible p53-regulated mediator of the G1 checkpoint in keratinocytes.C/EBPα是一种在角质形成细胞中受DNA损伤诱导且受p53调控的G1期检查点介质。
Mol Cell Biol. 2004 Dec;24(24):10650-60. doi: 10.1128/MCB.24.24.10650-10660.2004.

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