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补骨脂素加紫外线A(PUVA)诱导的早衰作为应激诱导早衰的模型。

Psoralen plus UVA (PUVA) induced premature senescence as a model for stress-induced premature senescence.

作者信息

Ma Wenjian, Wlaschek Meinhard, Hommel Christina, Schneider Lars Alexander, Scharffetter-Kochanek Karin

机构信息

Department of Dermatology and Allergy, University of Ulm, Maienweg 12, 89081 Ulm, Germany.

出版信息

Exp Gerontol. 2002 Oct-Nov;37(10-11):1197-201. doi: 10.1016/s0531-5565(02)00143-2.

Abstract

Following psoralen photoactivation (PUVA treatment) human dermal fibroblasts undergo long-term growth arrest as well as morphological and functional changes reminiscent of replicative senescence. Although the molecular description of cellular senescence is still incomplete, replicative senescence of cultured human cells has been suggested to reflect cellular aging in vitro. Recently, the term stress-induced premature senescence (SIPS) was introduced to define in vitro models with longterm growth arrest upon exposure to sublethal stressors (i.e. hyperoxia, hydrogen peroxide, ethanol), which are characterized by morphological and functional changes common for replicative senescence. This mini review focuses on the morphological and functional changes in the fibroblast phenotype following exposure to psoralen plus UVA (PUVA) leading to SIPS and the role of reactive oxygen species in the switch from the proliferative to the post mitotic cell. Additionally, we will discuss the possible in vivo relevance of PUVA-SIPS fibroblasts in PUVA-treated patients.

摘要

在补骨脂素光活化(PUVA治疗)后,人皮肤成纤维细胞会经历长期生长停滞以及形态和功能变化,这些变化让人联想到复制性衰老。尽管细胞衰老的分子描述仍不完整,但培养的人细胞的复制性衰老被认为反映了体外细胞衰老。最近,引入了“应激诱导的早衰(SIPS)”一词来定义在暴露于亚致死应激源(即高氧、过氧化氢、乙醇)后出现长期生长停滞的体外模型,这些模型的特征是具有复制性衰老常见的形态和功能变化。这篇小型综述重点关注暴露于补骨脂素加紫外线A(PUVA)导致SIPS后成纤维细胞表型的形态和功能变化,以及活性氧在从增殖细胞向有丝分裂后细胞转变中的作用。此外,我们将讨论PUVA-SIPS成纤维细胞在接受PUVA治疗的患者体内可能的相关性。

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