Delivery of alginate-chitosan hydrogel promotes endogenous repair and preserves cardiac function in rats with myocardial infarction
The regenerative potential of alginate‐chitosan composite in bone and cartilage tissue has been well documented, but its potential utility in cardiac tissue engineering has remained unknown. This study sought to determine whether early intramyocardial injection of alginate‐chitosan could prevent lef...
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Published in | Journal of biomedical materials research. Part A Vol. 103; no. 3; pp. 907 - 918 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Blackwell Publishing Ltd
01.03.2015
Wiley Subscription Services, Inc |
Subjects | |
Online Access | Get full text |
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Summary: | The regenerative potential of alginate‐chitosan composite in bone and cartilage tissue has been well documented, but its potential utility in cardiac tissue engineering has remained unknown. This study sought to determine whether early intramyocardial injection of alginate‐chitosan could prevent left ventricular (LV) remodeling after myocardial infarction (MI), leading to a more favorable course of tissue restoration. In a rat model of acute MI, local injection of alginate‐chitosan hydrogel into the peri‐infarct zone preserved scar thickness, attenuated infarct expansion, and reduced scar fibrosis after 8 weeks, concomitantly with promoting increased angiogenesis and greater recruitment of endogenous repair at the infarct zone. Furthermore, this treatment prevented cell apoptosis, induced cardiomyocyte cell cycle re‐entry. The cardiac function of the control‐injected animals deteriorated over the 8‐week course, while that of the hydrogel‐injected animals did not.In addition, the hydrogel did not exacerbate inflammation in the heart. Intramyocardial injection of alginate‐chitosan hydrogel represents a useful strategy to treat MI. It demonstrated marked therapeutic efficacies on various tissue levels after extensive MI, as well as potential to induce endogenous cardiomyocyte proliferation and recruit cardiac stem cells. © 2014 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 103A: 907–918, 2015. |
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Bibliography: | istex:D9D46FC3CF3EB138477ABA0CAC7BAA33E033135C ark:/67375/WNG-G2BD9Q7Q-8 Conflict of Interest: The authors declare no competing financial interest. ArticleID:JBMA35232 These authors contributed equally to this work. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1549-3296 1552-4965 |
DOI: | 10.1002/jbm.a.35232 |