Exp Dermatol. 2011 Oct;20(10):836-8. doi: 10.1111/j.1600-0625.2011.01324.x. Epub 2011 Jun 26.
Oxidative stress is one of the most important causes of the cellular senescence process. Previous studies showed that β-catenin can regulate FoxO3a and this association was enhanced in cells exposed to oxidative stress. It has also been reported that β-catenin can regulate some senescence-related proteins. We propose that β-catenin may play a crucial role in senescence of normal human primary skin fibroblasts (NHSFs). Here, we explored the roles and mechanisms of β-catenin on H(2)O(2)-induced senescence in NHSFs. β-catenin expression was decreased in NHSFs after H(2)O(2) treatment. Overexpression of β-catenin in NHSFs led to a marked delay of many senescent phenotypes induced by H(2)O(2). Furthermore, overexpression of β-catenin in NHSFs can antagonise the alteration of reactive oxygen species accumulation and some senescence-related proteins expression induced by H(2)O(2) treatment. Our data demonstrated that β-catenin can protect NHSFs from H(2)O(2)-induced premature senescence by alleviating oxidative stress and regulating some senescence-related molecules.
氧化应激是细胞衰老过程的最重要原因之一。以前的研究表明β-catenin 可以调节 FoxO3a，并且这种关联在暴露于氧化应激的细胞中增强。也有报道称β-catenin 可以调节一些与衰老相关的蛋白质。我们提出β-catenin 可能在正常人类原代皮肤成纤维细胞（NHSFs）的衰老中起关键作用。在这里，我们探讨了β-catenin 在 NHSFs 中 H（2）O（2）诱导的衰老中的作用和机制。H（2）O（2）处理后 NHSFs 中的β-catenin 表达降低。在 NHSFs 中过表达β-catenin 会导致 H（2）O（2）诱导的许多衰老表型明显延迟。此外，在 NHSFs 中过表达β-catenin 可以拮抗 H（2）O（2）处理诱导的活性氧积累和一些与衰老相关的蛋白质表达的改变。我们的数据表明，β-catenin 通过减轻氧化应激和调节一些与衰老相关的分子来保护 NHSFs 免受 H（2）O（2）诱导的过早衰老。
