SMARCD1 regulates senescence-associated lipid accumulation in hepatocytes.

IF 5.4 Q1 GERIATRICS & GERONTOLOGY

NPJ Aging and Mechanisms of Disease Pub Date : 2017-08-30 eCollection Date: 2017-01-01 DOI:10.1038/s41514-017-0011-1

Chisato Inoue, Chong Zhao, Yumi Tsuduki, Miyako Udono, Lixiang Wang, Masatoshi Nomura, Yoshinori Katakura

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引用次数: 1

Abstract

Previously, we have identified 16 senescence-associated genes by a subtractive proteomic analysis using presenescent and senescent human fibroblast cells, TIG-1. The aim of this study was to clarify the role of SMARCD1, one of the identified genes, also known as BAF60a, in hepatic senescence. SMARCD1 is a member of the SWI/SNF chromatin remodeling complex family, and regulates the transcription of target genes through the alterations of chromatin structure. We demonstrated that the reduced expression of SMARCD1 triggers cellular senescence and induces the accumulation of lipids, suggesting that SMARCD1 acts as a mediator in these processes. Furthermore, palmitic acid treatment and high-fat diet led to a significant reduction of SMARCD1 expression, and consequently induced cellular senescence and lipid accumulation in HepG2 cells and mouse liver, respectively. The results obtained here suggest that dietary nutrient-associated impaired expression of SMARCD1 triggers cellular senescence and lipid accumulation, indicating a potential application of SMARCD1 in the prevention of lifestyle-related diseases.

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SMARCD1调节肝细胞中与衰老相关的脂质积累。

在此之前，我们利用现生和衰老的人成纤维细胞TIG-1，通过减法蛋白质组学分析鉴定了16个衰老相关基因。这项研究的目的是阐明SMARCD1在肝衰老中的作用，SMARCD1是鉴定出的基因之一，也被称为BAF60a。SMARCD1是SWI/SNF染色质重塑复合体家族的成员，通过改变染色质结构调控靶基因的转录。我们证明，SMARCD1的表达减少会触发细胞衰老并诱导脂质积累，这表明SMARCD1在这些过程中起着中介作用。此外，棕榈酸处理和高脂肪饮食导致SMARCD1表达显著降低，从而分别诱导HepG2细胞和小鼠肝脏的细胞衰老和脂质积累。本研究结果表明，膳食营养相关的SMARCD1表达受损会引发细胞衰老和脂质积累，这表明SMARCD1在预防生活方式相关疾病中的潜在应用。

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来源期刊

NPJ Aging and Mechanisms of Disease Medicine-Geriatrics and Gerontology

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审稿时长

8 weeks

期刊介绍： npj Aging and Mechanisms of Disease is an online open access journal that provides a forum for the world’s most important research in the fields of aging and aging-related disease. The journal publishes papers from all relevant disciplines, encouraging those that shed light on the mechanisms behind aging and the associated diseases. The journal’s scope includes, but is not restricted to, the following areas (not listed in order of preference): • cellular and molecular mechanisms of aging and aging-related diseases • interventions to affect the process of aging and longevity • homeostatic regulation and aging • age-associated complications • translational research into prevention and treatment of aging-related diseases • mechanistic bases for epidemiological aspects of aging-related disease.