| Periostin induces proliferation of differentiated cardiomyocytes and promotes cardiac repair. | |
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MedLine Citation:
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PMID: 17632525 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Adult mammalian hearts respond to injury with scar formation and not with cardiomyocyte proliferation, the cellular basis of regeneration. Although cardiogenic progenitor cells may maintain myocardial turnover, they do not give rise to a robust regenerative response. Here we show that extracellular periostin induced reentry of differentiated mammalian cardiomyocytes into the cell cycle. Periostin stimulated mononucleated cardiomyocytes to go through the full mitotic cell cycle. Periostin activated alphaV, beta1, beta3 and beta5 integrins located in the cardiomyocyte cell membrane. Activation of phosphatidylinositol-3-OH kinase was required for periostin-induced reentry of cardiomyocytes into the cell cycle and was sufficient for cell-cycle reentry in the absence of periostin. After myocardial infarction, periostin-induced cardiomyocyte cell-cycle reentry and mitosis were associated with improved ventricular remodeling and myocardial function, reduced fibrosis and infarct size, and increased angiogenesis. Thus, periostin and the pathway that it regulates may provide a target for innovative strategies to treat heart failure. |
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Authors:
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Bernhard Kühn; Federica del Monte; Roger J Hajjar; Yuh-Shin Chang; Djamel Lebeche; Shima Arab; Mark T Keating |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2007-07-15 |
Journal Detail:
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Title: Nature medicine Volume: 13 ISSN: 1078-8956 ISO Abbreviation: Nat. Med. Publication Date: 2007 Aug |
Date Detail:
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Created Date: 2007-08-07 Completed Date: 2007-10-17 Revised Date: 2007-12-03 |
Medline Journal Info:
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Nlm Unique ID: 9502015 Medline TA: Nat Med Country: United States |
Other Details:
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Languages: eng Pagination: 962-9 Citation Subset: IM |
Affiliation:
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Department of Cardiology, Children's Hospital Boston, 300 Longwood Avenue, Boston, Massachusetts 02115, USA. bernhard.kuhn@cardio.chboston.org |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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1-Phosphatidylinositol 3-Kinase
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metabolism Animals Cell Adhesion Molecules / pharmacology*, therapeutic use Cell Differentiation* / drug effects Cell Proliferation / drug effects Cells, Cultured DNA / biosynthesis Fibrosis / drug therapy, pathology Humans Hypertrophy / drug therapy, pathology Integrins / metabolism Male Myocardial Infarction / drug therapy, physiopathology Myocytes, Cardiac / cytology*, drug effects*, physiology Rats Rats, Wistar Regeneration / drug effects* |
| Grant Support | |
ID/Acronym/Agency:
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HL057263/HL/NHLBI NIH HHS; HL071763/HL/NHLBI NIH HHS; HL080498/HL/NHLBI NIH HHS; HL083156/HL/NHLBI NIH HHS; K01 HL076659/HL/NHLBI NIH HHS; K08 HL069842/HL/NHLBI NIH HHS; R01 HL078691/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Cell Adhesion Molecules; 0/Integrins; 9007-49-2/DNA; EC 2.7.1.137/1-Phosphatidylinositol 3-Kinase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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