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Nucleostemin exerts anti-apoptotic function via p53 signaling pathway in cardiomyocytes
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  • 作者:Chi Zhang ; Jiahai Shi ; Long Qian ; Chao Zhang
  • 关键词:Nucleostemin ; Apoptosis ; p53 ; Myocardial ischemia reperfusion
  • 刊名:In Vitro Cellular & Developmental Biology - Animal
  • 出版年:2015
  • 出版时间:November 2015
  • 年:2015
  • 卷:51
  • 期:10
  • 页码:1064-1071
  • 全文大小:3,673 KB
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  • 作者单位:Chi Zhang (1) (4)
    Jiahai Shi (2) (4)
    Long Qian (2) (4)
    Chao Zhang (1) (4)
    Kunpeng Wu (2) (4)
    Chen Yang (2) (4)
    Daliang Yan (2) (4)
    Xiang Wu (1) (4)
    Xiaojuan Liu (3) (4)

    1. Department of Cardiology, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, People鈥檚 Republic of China
    4. Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College, Nantong University, Nantong, 226001, Jiangsu, People鈥檚 Republic of China
    2. Department of Thoracic Surgery, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, People鈥檚 Republic of China
    3. Department of Pathogen Biology, Medical College, Nantong University, Nantong, 226001, Jiangsu, People鈥檚 Republic of China
  • 刊物主题:Cell Biology; Developmental Biology; Stem Cells; Cell Culture; Animal Genetics and Genomics;
  • 出版者:Springer US
  • ISSN:1543-706X
文摘
Cardiomyocytes apoptosis following reperfusion injury causes irreversible damage to cardiac function. Understanding the mechanisms underlying cardiomyocytes death under these conditions can be helpful to identify strategies to abrogate such detrimental effects. Stem cell-specific proteins and regulatory pathways become important in understanding reparative processes in the myocardium. One such regulatory protein named nucleostemin (NS) has vital roles in cardiac ischemia. Although the relationship between NS and cell apoptosis has been studied, it is unknown how NS is controlled and how it participates in cardiomyocytes apoptosis induced by ischemia reperfusion (I/R). In the present study, we aimed to investigate the direct role of NS in myocardial I/R. In vivo, NS was highly expressed in cardiac tissues after I/R. Double immunofluorescent staining showed that NS located in the nucleolar of cardiomyocytes and correlated with cardiomyocytes apoptosis. Furthermore, in vitro primary rat cardiomyocytes increased NS expression induced by hypoxia-reoxygenation (H/R) treatment, in line with results in vivo. Suppression of NS expression by siNS promoted the expression of terminal deoxynucleotide transferase-mediated dUTP nick end labeling (TUNEL)-positive cells p53 and cleaved caspase-3, which demonstrates I/R may require increased expression of NS to suppress p53 activation and maintain cardiomyocytes survival. Keywords Nucleostemin Apoptosis p53 Myocardial ischemia reperfusion

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