MiR-126-3p and MiR-199a-3p Promote Lipid Accumulation in 3T3-L1 Adipocytes via Regulating HIF-1α and C/EBPα Expression

アクセス数 : 2247
ダウンロード数 : 111

今月のアクセス数 : 77
今月のダウンロード数 : 0
ファイル情報(添付)
タイトル
MiR-126-3p and MiR-199a-3p Promote Lipid Accumulation in 3T3-L1 Adipocytes via Regulating HIF-1α and C/EBPα Expression
著者
JAHAN Israt
中島 淳
収録物名
Shimane Journal of Medical Science
39
4
開始ページ 123
終了ページ 133
収録物識別子
ISSN 03865959
EISSN 24332410
内容記述
その他
Non-alcoholic fatty liver disease (NAFLD) is one major chronic liver disease emerging the primarily excessive fat accumulation in the liver. Recent studies have demonstrated that hepatic miRNAs play an important role of NAFLD pathogenesis. Previously we identified up-regulation of miR-126-3p and miR-199a-3p in the patient with NAFLD, but their roles remain unclear. In this study, we investigated the role of miR-126-3p and miR-199a-3p on lipid accumulation in 3T3-L1 adipocytes. Transfection of miR-126-3p and miR-199a-3p enhanced lipid accumulation in 3T3-L1 cells after adipocyte differentiation. Next, we evaluated lipid metabolism-related gene expression by quantitative RT-PCR. MiR-126-3p increased CCAAT/enhancer-binding protein-α (C/EBPα) mRNA expression whereas miR-199a-3p did not affect. Moreover, both miRNAs reduced the expression of hypoxia-inducible factor-1α (HIF-1α) mRNA, predicted target of miRNAs. These results suggested that miR-126-3p and miR-199a-3p promote lipid accumulation in 3T3-L1 adipocytes through regulating HIF-1α and/or C/EBPα mRNA expression.
主題
Non-alcoholic fatty liver disease ( その他)
microRNA- 126-3p ( その他)
microRNA-199a-3p ( その他)
lipid deposition ( その他)
CCAAT/enhancer binding protein-α ( その他)
hypoxia-inducible factor-1α ( その他)
言語
英語
資源タイプ 紀要論文
出版者
Faculty of Medicine, Shimane University
島根大学医学部
発行日 2022-12
権利情報
Faculty of Medicine, Shimane University
権利関係(リンク) Creative Commons License
This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
出版タイプ Version of Record(出版社版。早期公開を含む)
アクセス権 オープンアクセス
関連情報
[NCID] AA00841586
[DOI] 10.51010/sjms.39.4_123