TY - JOUR
T1 - SMARCD1 regulates senescence-associated lipid accumulation in hepatocytes
AU - Inoue, Chisato
AU - Zhao, Chong
AU - Tsuduki, Yumi
AU - Udono, Miyako
AU - Wang, Lixiang
AU - Nomura, Masatoshi
AU - Katakura, Yoshinori
N1 - Funding Information:
The authors like to thank N. Oshima (GE Healthcare) for her expert assistance with the IN Cell Analyzer 1000. This work was supported in part by JSPS KAKENHI Grant Number 24580190.
Publisher Copyright:
© 2017, The Author(s).
PY - 2017/12/1
Y1 - 2017/12/1
N2 - 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.
AB - 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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U2 - 10.1038/s41514-017-0011-1
DO - 10.1038/s41514-017-0011-1
M3 - Article
AN - SCOPUS:85048133333
SN - 2056-3973
VL - 3
JO - npj Aging and Mechanisms of Disease
JF - npj Aging and Mechanisms of Disease
IS - 1
M1 - 11
ER -
