p300 inhibition delays premature cellular senescence.

IF 4.1 Q2 GERIATRICS & GERONTOLOGY
Elisabetta Di Fede, Esi Taci, Silvia Castiglioni, Stefano Rebellato, Silvia Ancona, Paolo Grazioli, Chiara Parodi, Elisa Adele Colombo, Clara Bernardelli, Elena Lesma, Ian Daniel Krantz, Stefania Corti, Alberto Priori, Grazia Fazio, Cristina Gervasini, Valentina Massa, Antonella Lettieri
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引用次数: 0

Abstract

Cellular senescence represents a permanent state of cell cycle arrest, also observed in neurodegenerative disorders. As p300 has been identified as an epigenetic driver of replicative senescence, we aimed to investigate whether in vitro p300 inhibition could rescue the stress-induced premature senescence (SIPS) phenotype. We exploited 2D and 3D (brain organoids) in vitro models of SIPS using two different stressor agents. In addition, we combined the treatment with a p300 inhibitor and validated p300 role in SIPS by analyzing different senescence markers and the transcriptome in our models. Interestingly, p300 inhibition can counteract the DNA damage and SIPS phenotype, detecting a dysregulation of gene expression and protein translation associated with the senescence program. These findings highlight both the molecular mechanisms underlying senescence and p300 as a possible pharmacological target. Thus, targeting p300 and, by extension, senescent cells could represent a promising therapeutic strategy for age-related diseases such as neurodegenerative disorders.

抑制P300延缓细胞过早衰老。
细胞衰老是细胞周期停滞的一种永久性状态,也见于神经退行性疾病。由于p300已被确定为复制性衰老的表观遗传驱动因子,我们旨在研究体外抑制p300是否可以挽救应激诱导的早衰(SIPS)表型。我们利用两种不同的应激剂在体外建立了SIPS的2D和3D(脑类器官)模型。此外,我们将治疗与p300抑制剂联合使用,并通过分析模型中不同的衰老标记物和转录组来验证p300在SIPS中的作用。有趣的是,p300抑制可以抵消DNA损伤和SIPS表型,检测与衰老程序相关的基因表达和蛋白质翻译失调。这些发现强调了衰老的分子机制和p300作为可能的药理学靶点。因此,靶向p300,进而扩展到衰老细胞,可能代表了一种有前途的治疗策略,用于治疗与年龄相关的疾病,如神经退行性疾病。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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CiteScore
8.90
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