Document Detail


MicroRNA-155 prevents necrotic cell death in human cardiomyocyte progenitor cells via targeting RIP1.
MedLine Citation:
PMID:  20550618     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
To improve regeneration of the injured myocardium, cardiomyocyte progenitor cells (CMPCs) have been put forward as a potential cell source for transplantation therapy. Although cell transplantation therapy displayed promising results, many issues need to be addressed before fully appreciating their impact. One of the hurdles is poor graft-cell survival upon injection, thereby limiting potential beneficial effects. Here, we attempt to improve CMPCs survival by increasing microRNA-155 (miR-155) levels, potentially to improve engraftment upon transplantation. Using quantitative PCR, we observed a 4-fold increase of miR-155 when CMPCs were exposed to hydrogen-peroxide stimulation. Flow cytometric analysis of cell viability, apoptosis and necrosis showed that necrosis is the main cause of cell death. Overexpressing miR-155 in CMPCs revealed that miR-155 attenuated necrotic cell death by 40 ± 2.3%via targeting receptor interacting protein 1 (RIP1). In addition, inhibiting RIP1, either by pre-incubating the cells with a RIP1 specific inhibitor, Necrostatin-1 or siRNA mediated knockdown, reduced necrosis by 38 ± 2.5% and 33 ± 1.9%, respectively. Interestingly, analysing gene expression using a PCR-array showed that increased miR-155 levels did not change cell survival and apoptotic related gene expression. By targeting RIP1, miR-155 repressed necrotic cell death of CMPCs, independent of activation of Akt pro-survival pathway. MiR-155 provides the opportunity to block necrosis, a conventionally thought non-regulated process, and might be a potential novel approach to improve cell engraftment for cell therapy.
Authors:
Jia Liu; Alain van Mil; Krijn Vrijsen; Jiajun Zhao; Ling Gao; Corina H G Metz; Marie-José Goumans; Pieter A Doevendans; Joost P G Sluijter
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-06-09
Journal Detail:
Title:  Journal of cellular and molecular medicine     Volume:  15     ISSN:  1582-4934     ISO Abbreviation:  J. Cell. Mol. Med.     Publication Date:  2011 Jul 
Date Detail:
Created Date:  2011-06-23     Completed Date:  2011-11-15     Revised Date:  2012-06-27    
Medline Journal Info:
Nlm Unique ID:  101083777     Medline TA:  J Cell Mol Med     Country:  England    
Other Details:
Languages:  eng     Pagination:  1474-82     Citation Subset:  IM    
Copyright Information:
© 2011 The Authors Journal of Cellular and Molecular Medicine © 2011 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.
Affiliation:
Department of Endocrinology, Provincial Hospital/Shandong University, Jinan, China.
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MeSH Terms
Descriptor/Qualifier:
Cell Death / physiology*
Cell Survival
Cells, Cultured
Humans
Imidazoles / metabolism
Indoles / metabolism
MicroRNAs / genetics,  metabolism*
Myocytes, Cardiac / cytology,  physiology*
Necrosis / metabolism*
Oxidative Stress
Phosphatidylinositol 3-Kinases / genetics,  metabolism
Proto-Oncogene Proteins c-akt / genetics,  metabolism
RNA, Small Interfering / genetics,  metabolism
Receptor-Interacting Protein Serine-Threonine Kinases / genetics,  metabolism*
Signal Transduction / physiology
Stem Cells / cytology,  physiology*
Chemical
Reg. No./Substance:
0/Imidazoles; 0/Indoles; 0/MIRN155 microRNA, human; 0/MicroRNAs; 0/RNA, Small Interfering; 0/necrostatin-1; EC 2.7.1.-/Phosphatidylinositol 3-Kinases; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.11.1/RIPK1 protein, human; EC 2.7.11.1/Receptor-Interacting Protein Serine-Threonine Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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