ヤマト　マサユキ   YAMATO Masayuki   大和　雅之    所属   研究施設 研究施設    職種   教授
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	Enhanced Migration of murin fibroblast-like 3T3-L1 preadipocytes on type I collagen-coated dish is reversed by silibinin treatment.
掲載誌名	正式名：Molecular and cellular biochemistry 略　 称：Mol Cell Biochem ISSNコード：(1573-4919)0300-8177(Linking)
掲載区分	国外
出版社	Springer
巻・号・頁	441(1-2),pp.35-62
著者・共著者	LIU Xiaoling†, XU Qian, YAO Guodong, YELI Zhao, XU Fanxing, HAYASHI Toshihiko, FUJISAKI Hitomi, HATTORI Shunji, TASHIRO Shin-ichi, ONODERA Satoshi, YAMATO Masayuki, IKEJIMA Takashi*
発行年月	2018/04
概要	Migration of fibroblast-like preadipocytes is important for the development of adipose tissue, whereas excessive migration is often responsible for impaired adipose tissue related with obesity and fibrotic diseases. Type I collagen (collagen I) is the most abundant component of extracellular matrix and has been shown to regulate fibroblast migration in vitro, but its role in adipose tissue is not known. Silibinin is a bioactive natural flavonoid with antioxidant and antimetastasis activities. In this study, we found that type I collagen coating promoted the proliferation and migration of murine 3T3-L1 preadipocytes in a dose-dependent manner, implying that collagen I could be an extracellular signal. Regarding the mechanisms of collagen I-stimulated 3T3-L1 migration, we found that NF-κB p65 is activated, including the increased nuclear translocation of NF-κB p65 as well as the upregulation of NF-κB p65 phosphorylation and acetylation, accompanied by the increased expressions of proinflammatory factors and the generation of reactive oxygen species (ROS). Reduction of collagen I-enhanced migration of cells by treatment with silibinin was associated with suppression of NF-κB p65 activity and ROS generation, and negatively correlated with the increasing sirt1 expression. Taken together, the enhanced migration of 3T3-L1 cells induced on collagen I-coated dish is mediated by the activation of NF-κB p65 function and ROS generation that can be alleviated with silibinin by upregulation of sirt1, leading to the repression of NF-κB p65 function and ROS generation.
DOI	10.1007/s11010-017-3173-z
PMID	28933025