Insulin and LiCl synergistically rescue myogenic differentiation of FoxO1 over-expressed myoblasts

NCUIR > college of Health Sciences and Technology > Department of Life Science > journal & Dissertation > Item 987654321/102579

Please use this identifier to cite or link to this item: https://ir.lib.ncu.edu.tw/handle/987654321/102579

Title:	Insulin and LiCl synergistically rescue myogenic differentiation of FoxO1 over-expressed myoblasts
Authors:	陳盛良;Wu, Yi Ju;Fang, Yen Hsin;Chi, Hsiang Cheng;Chang, Li Chiung;Chung, Shih Ying;Huang, Wei Chieh;Wang, Xiao Wen;Lee, Kuan Wei;Chen, Shen Liang
Contributors:	生醫理工學院生命科學系
Keywords:	Accumulation;Active Transport, Cell Nucleus - drug effects;Animals;Autophagy;Biology;Cell cycle;Cell Differentiation - drug effects;Cell Line;Cell Nucleus - drug effects;Cell Nucleus - metabolism;Culture Media;Cytosol - drug effects;Cytosol - metabolism;Deprivation;Differentiation;Endocrinology;Fatty Acids, Unsaturated - pharmacology;Forkhead Box Protein O1;Forkhead Transcription Factors - genetics;Forkhead Transcription Factors - metabolism;FOXO1 protein;Gene Expression Regulation;Gene silencing;Glucose;Hypertrophy;Insulin;Insulin - pharmacology;Kinases;Leptomycin B;Life sciences;Lithium chloride;Lithium Chloride - pharmacology;Mammals;Mice;Muscle Development - drug effects;Muscle Development - genetics;Muscle Fibers, Skeletal - cytology;Muscle Fibers, Skeletal - drug effects;Muscle Fibers, Skeletal - metabolism;Musculoskeletal system;Myoblasts;Myoblasts - cytology;Myoblasts - drug effects;Myoblasts - metabolism;Myogenesis;Myogenic Regulatory Factors - genetics;Myogenic Regulatory Factors - metabolism;Myotubes;Nuclear transport;Overexpression;Phosphorylation;Promoter Regions, Genetic;Proteins;Rodents;Serum - chemistry;Signal Transduction;Signaling;Transcription factors;Wnt protein;Wnt Proteins - genetics;Wnt Proteins - metabolism
Date:	2014-02-13
Issue Date:	2026-04-23 11:13:09 (UTC+8)
Publisher:	Public Library of Science;United States: Public Library of Science (PLoS)
Abstract:	摘要： Most recent studies reported that FoxO1 transcription factor was a negative regulator of myogenesis under serum withdrawal condition, a situation not actually found in vivo. Therefore, the role of FoxO1 in myogenesis should be re-examined under more physiologically relevant conditions. Here we found that FoxO1 was preferentially localized to nucleus in proliferating (PMB) and confluent myoblasts (CMB) and its nuclear exclusion was a prerequisite for formation of multinucleated myotubes (MT). The nuclear shuttling of FoxO1 in PMB could be prevented by leptomycin B and we further found that cytoplasmic accumulation of FoxO1 in myotubes was caused by the blockade of its nuclear import. Although over-expression of wildtype FoxO1 in C2C12 myoblasts significantly blocked their myogenic differentiation under serum withdrawal condition, application of insulin and LiCl, an activator of Wnt signaling pathway, to these cells successfully rescued their myogenic differentiation and generated myotubes with larger diameters. Interestingly, insulin treatment significantly reduced FoxO1 level and also delayed nuclear re-accumulation of FoxO1 triggered by mitogen deprivation. We further found that FoxO1 directly repressed the promoter activity of myogenic genes and this repression can be relieved by insulin and LiCl treatment. These results suggest that FoxO1 inhibits myogenesis in serum withdrawal condition but turns into a hypertrophy potentiator when other myogenic signals, such as Wnt and insulin, are available. 其他題名： PLoS One 出版者： United States: Public Library of Science (PLoS) 出版日期： 2014-02-13 出處： PLoS ONE, 2014-02, Vol.9 (2), p.e88450- 資源來源： Agricultural & Environmental Science Collection 版權： COPYRIGHT 2014 Public Library of Science 版權： 2014 Wu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 版權： 2014 Wu et al 2014 Wu et al 識別號： ISSN: 1932-6203 識別號： EISSN: 1932-6203 識別號： DOI: 10.1371/journal.pone.0088450 識別號： PMID: 24551104
Appears in Collections:	[Department of Life Science] journal & Dissertation

Files in This Item:

File	Description	Size	Format
index.html		0Kb	HTML	15	View/Open

社群 sharing

Loading...