Die Meng 1 , Seongho Han 1 , In Sil Jeong 2 , Sung-Whan Kim 2,3 . Show Affiliations »
Abstract
BACKGROUND/AIMS: Stem cells or progenitor cells have been demonstrated as a novel alternative for cell therapy; however, their sustained efficacy is still debated. This study aimed to evaluate whether interleukin 10 (IL-10) gene-edited amniotic mesenchymal stem cells (AMM/I) contribute to left ventricular (LV) function and remodeling after acute myocardial infarction (AMI). METHODS: The IL-10 gene was integrated into the genomic locus of AMM via transcription activator-like effector nucleases (TALEN) and AMM/I were intramyocardially transplanted into AMI mice models. Cardiac function, quantitative polymerase chain reaction, histology, capillary density, and apoptosis assays were performed. RESULTS: AMM/I transplantation significantly suppressed infiltrated CD68 positive or F4/80 positive inflammatory cells and reduced the expression of pro-inflammatory factors in the infarcted myocardium. In addition, significantly improved LV function and reduced infarct size was noted in mice model with AMM/I transplantation than in those given AMM. Moreover, AMM/I highly inhibited cell apoptosis and increased capillary density in the infarcted myocardium. CONCLUSION: Our study demonstrated that AMM/I recruitment played favorable roles in the early restoration of LV function and remodeling by suppressing inflammation and enhancing cardiac protection and capillary density. © Copyright by the Author(s). Published by Cell Physiol Biochem Press.
BACKGROUND/AIMS: Stem cells or progenitor cells have been demonstrated as a novel alternative for cell therapy; however, their sustained efficacy is still debated. This study aimed to evaluate whether interleukin 10 (IL-10 ) gene-edited amniotic mesenchymal stem cells (AMM/I) contribute to left ventricular (LV) function and remodeling after acute myocardial infarction (AMI). METHODS: The IL-10 gene was integrated into the genomic locus of AMM via transcription activator-like effector nucleases (TALEN) and AMM/I were intramyocardially transplanted into AMI mice models. Cardiac function, quantitative polymerase chain reaction, histology, capillary density, and apoptosis assays were performed. RESULTS: AMM/I transplantation significantly suppressed infiltrated CD68 positive or F4/80 positive inflammatory cells and reduced the expression of pro-inflammatory factors in the infarcted myocardium . In addition, significantly improved LV function and reduced infarct size was noted in mice model with AMM/I transplantation than in those given AMM. Moreover, AMM/I highly inhibited cell apoptosis and increased capillary density in the infarcted myocardium . CONCLUSION: Our study demonstrated that AMM/I recruitment played favorable roles in the early restoration of LV function and remodeling by suppressing inflammation and enhancing cardiac protection and capillary density. © Copyright by the Author(s). Published by Cell Physiol Biochem Press.
Entities: Disease
Gene
Species
Keywords:
Acute myocardial infarction; Amniotic mesenchymal stem cells; Anti-inflammation; Cardiac remodeling; Genome editing
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Substances: See more »
Year: 2019
PMID: 30921510 DOI: 10.33594/000000051
Source DB: PubMed Journal: Cell Physiol Biochem ISSN: 1015-8987