Acellular Human Amniotic Membrane Scaffold with 15d-PGJ 2 Nanoparticles in Postinfarct Rat Model
The difficulty in the regeneration of cardiomyocytes after myocardial infarction is a major cause of heart failure. Together, the amniotic membrane and 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ ) can help in the recovery of cardiomyocyte, as they present many growth factors and anti-inflammatory eff...
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Published in | Tissue engineering. Part A Vol. 26; no. 21-22; p. 1128 |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
01.11.2020
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Subjects | |
Online Access | Get more information |
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Summary: | The difficulty in the regeneration of cardiomyocytes after myocardial infarction is a major cause of heart failure. Together, the amniotic membrane and 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ
) can help in the recovery of cardiomyocyte, as they present many growth factors and anti-inflammatory effect, respectively. The objective of this study is to compare the efficacy of Human Decellularized Amniotic Membrane Scaffold (AHAS) loaded with 15d-PGJ
in improving ventricular function in a rat model of postinfarct ventricular dysfunction. Myocardial infarction was induced in 24 rats by left coronary occlusion. After a week, the animals were subjected to echocardiography for evaluation of left ventricle ejection fraction (LVEF), left ventricle end diastolic volume (LVEDV), and left ventricle end systolic volume (LVESV). Animals with ejection fraction <40% were included in the study and were randomized into three groups: control (
= 8), AHAS (
= 8) and AHAS +15d-PGJ
(
= 8). In the AHAS group only the membrane was implanted, whereas in the AHAS +15d-PGJ
the membrane +15d-PGJ
was implanted on myocardial infarction. Echocardiographic evaluation was performed after 1 month. For histological analysis, heart tissue was stained with Gomori trichome, Sirius Red, the antibody against CD31 and connexin 43 (Cx43). There were no significant differences in the baseline LVEF, LVEDV, and LVESV in all groups. After 1 month, ejection fraction decreased in the control group but increased in the AHAS group and in the AHAS +15d-PGJ
group in comparison with the control group. The LVEDV and LVESV in the AHAS and AHAS +15d-PGJ
groups decreased compared with the control group, featuring a ventricular antiremodeling effect. Histopathology of the infarcted area identified the reduction of infarct size and collagen type 1 in the AHAS and AHAS +15d-PGJ
groups. New blood vessels and cardiomyocytes have been identified in an infarcted area by CD31 and Cx43. AHAS +15d-PGJ
provided an increase in the ejection fraction and prevented ventricular dilation in this postinfarction ventricular dysfunction model. Impact Statement Our study demonstrated reduction of myocardial fibrosis, proliferation of cardiomyocytes and increase in ejection fraction in rats after experimental acellular amniotic membrane scaffold (AHAS) carrying nanoparticles of 15d-PGJ2 scaffold engraftment in infarcted myocardium. AHAS grafts facilitated colonization of fibrotic myocardium regions with new contractile cells, in addition to preventing reduction of left ventricle wall thickness. This contribution is theoretically and practically relevant as current literature describes experimental studies performed on cardiac ischemic models which present conflicting results concerning cell types used in a research model. |
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ISSN: | 1937-335X |
DOI: | 10.1089/ten.tea.2019.0340 |