科研成果详情

题名bFGF regulates autophagy and ubiquitinated protein accumulation induced by myocardial ischemia/reperfusion via the activation of the PI3K/Akt/mTOR pathway
作者
发表日期2015-03-19
发表期刊SCIENTIFIC REPORTS   影响因子和分区
语种英语
原始文献类型Article
其他关键词FIBROBLAST-GROWTH-FACTOR ; ISCHEMIA-REPERFUSION INJURY ; INDUCED CELL-DEATH ; PROTEASOME SYSTEM ; MAMMALIAN TARGET ; HEART ; P62 ; DISEASE ; STRESS ; ROLES
摘要Autophagy is involved in the development and/or progression of many diseases, including myocardial ischemia/reperfusion (I/R). In this study, we hypothesized a protective role of basic fibroblast growth factor (bFGF) both in vivo and in vitro and demonstrated that excessive autophagy and ubiquitinated protein accumulation is involved in the myocardial I/R model. Our results showed that bFGF improved heart function recovery and increased the survival of cardiomyocytes in myocardial I/R model. The protective effect of bFGF is related to the inhibition of LC3II levels. Additionally, bFGF enhances the clearance of Ub by p62 and increases the survival of H9C2 cells. Moreover, silencing of p62 partially blocks the clearance of Ub and abolishes the anti-apoptosis effect of bFGF. An shRNA against the autophagic machinery Atg7 increased the survival of H9C2 cells co-treated with bFGF and rapamycin. bFGF activates the downstream signaling of the PI3K/Akt/mTOR pathway. These results indicate that the role of bFGF in myocardial I/R recovery is related to the inhibition of excessive autophagy and increased ubiquitinated protein clearance via the activation of PI3K/Akt/mTOR signaling. Overall, our study suggests a new direction for bFGF drug development for heart disease and identifies protein signaling pathways involved in bFGF action.
资助项目National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [81302775, 81170203]; Zhejiang Provincial Program for the Cultivation of High-level Innovative Health talents; State Key Basic Research Development Program [2012CB518105]; Zhejiang Provincial Project of Protein Medicine Key Group [2010R50042]
出版者NATURE PUBLISHING GROUP
出版地LONDON
ISSN2045-2322
卷号5
DOI10.1038/srep09287
页数12
WOS类目Multidisciplinary Sciences
WOS研究方向Science & Technology - Other Topics
WOS记录号WOS:000351276500003
收录类别SCIE ; SCOPUS
URL查看原文
PubMed ID25787015
SCOPUSEID2-s2.0-84925356599
通讯作者地址[Chu, Mao-Ping]Department of Pediatric Cardiology, Second Affiliated Hospital, Wenzhou Medical University,Wenzhou,325000,China
Scopus学科分类Multidisciplinary
引用统计
被引频次:86[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符https://kms.wmu.edu.cn/handle/3ETUA0LF/10322
专题药学院(分析测试中心)
附属第二医院
第二临床医学院、附属第二医院、育英儿童医院
研究生工作部(研究生院)
第二临床医学院、附属第二医院、育英儿童医院_影像医学与核医学_超声科
药学院(分析测试中心)_生物制药系_生物制药工程
通讯作者Chu, Mao-Ping
作者单位
1.School of Pharmacy, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University,Wenzhou,325035,China;
2.Department of Biochemistry and Molecular Biology, College of Basic Medical Science, Jilin University,Changchun,130012,China;
3.Department of Pediatric Cardiology, Second Affiliated Hospital, Wenzhou Medical University,Wenzhou,325000,China;
4.Department of Ultrasound, Second Affiliated Hospital, Wenzhou Medical University,Wenzhou,325000,China;
5.Department of Medical Immunology, Medical School, Anhui University of Science and Technology,Huainan,232001,China;
6.Institute of Basic Medical Science, Chinese PLA General Hospital,Beijing,100853,China
第一作者单位药学院(分析测试中心)
通讯作者单位附属第二医院
第一作者的第一单位药学院(分析测试中心)
推荐引用方式
GB/T 7714
Wang, Zhou-Guang,Wang, Yue,Huang, Yan,et al. bFGF regulates autophagy and ubiquitinated protein accumulation induced by myocardial ischemia/reperfusion via the activation of the PI3K/Akt/mTOR pathway[J]. SCIENTIFIC REPORTS,2015,5.
APA Wang, Zhou-Guang., Wang, Yue., Huang, Yan., Lu, Qin., Zheng, Lei., ... & Xiao, Jian. (2015). bFGF regulates autophagy and ubiquitinated protein accumulation induced by myocardial ischemia/reperfusion via the activation of the PI3K/Akt/mTOR pathway. SCIENTIFIC REPORTS, 5.
MLA Wang, Zhou-Guang,et al."bFGF regulates autophagy and ubiquitinated protein accumulation induced by myocardial ischemia/reperfusion via the activation of the PI3K/Akt/mTOR pathway".SCIENTIFIC REPORTS 5(2015).

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