Cargando…
Exosomes from SIRT1-Overexpressing ADSCs Restore Cardiac Function by Improving Angiogenic Function of EPCs
Acute myocardial infarction (AMI) is one of the leading causes of mortality in cardiovascular diseases. The aim of this study was to investigate whether exosomes from Sirtuin 1 (SIRT1)-overexpressing adipose-derived stem cells (ADSCs) had a protective effect on AMI. The expression of C-X-C chemokine...
Autores principales: | , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Society of Gene & Cell Therapy
2020
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7412761/ https://www.ncbi.nlm.nih.gov/pubmed/32771925 http://dx.doi.org/10.1016/j.omtn.2020.07.007 |
_version_ | 1783568674140979200 |
---|---|
author | Huang, Hui Xu, Zhenxing Qi, Yuan Zhang, Wei Zhang, Chenjun Jiang, Mei Deng, Shengqiong Wang, Hairong |
author_facet | Huang, Hui Xu, Zhenxing Qi, Yuan Zhang, Wei Zhang, Chenjun Jiang, Mei Deng, Shengqiong Wang, Hairong |
author_sort | Huang, Hui |
collection | PubMed |
description | Acute myocardial infarction (AMI) is one of the leading causes of mortality in cardiovascular diseases. The aim of this study was to investigate whether exosomes from Sirtuin 1 (SIRT1)-overexpressing adipose-derived stem cells (ADSCs) had a protective effect on AMI. The expression of C-X-C chemokine receptor type 7 (CXCR7) was significantly downregulated in peripheral blood endothelial progenitor cells (EPCs) from AMI patients (AMI-EPCs) compared with that in healthy donors, which coincided with impaired tube formation. The exosomes from SIRT1 overexpression in ADSCs (ADSCs-SIRT1-Exos) increased the expression of C-X-C motif chemokine 12 (CXCL12) and nuclear factor E2 related factor 2 (Nrf2) in AMI-EPCs, which promoted migration and tube formation of AMI-EPCs, and overexpression of CXCR7 helped AMI-EPCs to restore the function of cell migration and tube formation. Moreover, CXCR7 was downregulated in the myocardium of AMI mice, and knockout of CXCR7 exacerbated AMI-induced impairment of cardiovascular function. Injection of ADSCs-SIRT1-Exos increased the survival and promoted the recovery of myocardial function with reduced infarct size and post-AMI left ventricular remodeling, induced vasculogenesis, and decreased AMI-induced myocardial inflammation. These findings showed that ADSCs-SIRT1-Exos may recruit EPCs to the repair area and that this recruitment may be mediated by Nrf2/CXCL12/CXCR7 signaling. |
format | Online Article Text |
id | pubmed-7412761 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | American Society of Gene & Cell Therapy |
record_format | MEDLINE/PubMed |
spelling | pubmed-74127612020-08-14 Exosomes from SIRT1-Overexpressing ADSCs Restore Cardiac Function by Improving Angiogenic Function of EPCs Huang, Hui Xu, Zhenxing Qi, Yuan Zhang, Wei Zhang, Chenjun Jiang, Mei Deng, Shengqiong Wang, Hairong Mol Ther Nucleic Acids Article Acute myocardial infarction (AMI) is one of the leading causes of mortality in cardiovascular diseases. The aim of this study was to investigate whether exosomes from Sirtuin 1 (SIRT1)-overexpressing adipose-derived stem cells (ADSCs) had a protective effect on AMI. The expression of C-X-C chemokine receptor type 7 (CXCR7) was significantly downregulated in peripheral blood endothelial progenitor cells (EPCs) from AMI patients (AMI-EPCs) compared with that in healthy donors, which coincided with impaired tube formation. The exosomes from SIRT1 overexpression in ADSCs (ADSCs-SIRT1-Exos) increased the expression of C-X-C motif chemokine 12 (CXCL12) and nuclear factor E2 related factor 2 (Nrf2) in AMI-EPCs, which promoted migration and tube formation of AMI-EPCs, and overexpression of CXCR7 helped AMI-EPCs to restore the function of cell migration and tube formation. Moreover, CXCR7 was downregulated in the myocardium of AMI mice, and knockout of CXCR7 exacerbated AMI-induced impairment of cardiovascular function. Injection of ADSCs-SIRT1-Exos increased the survival and promoted the recovery of myocardial function with reduced infarct size and post-AMI left ventricular remodeling, induced vasculogenesis, and decreased AMI-induced myocardial inflammation. These findings showed that ADSCs-SIRT1-Exos may recruit EPCs to the repair area and that this recruitment may be mediated by Nrf2/CXCL12/CXCR7 signaling. American Society of Gene & Cell Therapy 2020-07-10 /pmc/articles/PMC7412761/ /pubmed/32771925 http://dx.doi.org/10.1016/j.omtn.2020.07.007 Text en © 2020 The Author(s) http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Article Huang, Hui Xu, Zhenxing Qi, Yuan Zhang, Wei Zhang, Chenjun Jiang, Mei Deng, Shengqiong Wang, Hairong Exosomes from SIRT1-Overexpressing ADSCs Restore Cardiac Function by Improving Angiogenic Function of EPCs |
title | Exosomes from SIRT1-Overexpressing ADSCs Restore Cardiac Function by Improving Angiogenic Function of EPCs |
title_full | Exosomes from SIRT1-Overexpressing ADSCs Restore Cardiac Function by Improving Angiogenic Function of EPCs |
title_fullStr | Exosomes from SIRT1-Overexpressing ADSCs Restore Cardiac Function by Improving Angiogenic Function of EPCs |
title_full_unstemmed | Exosomes from SIRT1-Overexpressing ADSCs Restore Cardiac Function by Improving Angiogenic Function of EPCs |
title_short | Exosomes from SIRT1-Overexpressing ADSCs Restore Cardiac Function by Improving Angiogenic Function of EPCs |
title_sort | exosomes from sirt1-overexpressing adscs restore cardiac function by improving angiogenic function of epcs |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7412761/ https://www.ncbi.nlm.nih.gov/pubmed/32771925 http://dx.doi.org/10.1016/j.omtn.2020.07.007 |
work_keys_str_mv | AT huanghui exosomesfromsirt1overexpressingadscsrestorecardiacfunctionbyimprovingangiogenicfunctionofepcs AT xuzhenxing exosomesfromsirt1overexpressingadscsrestorecardiacfunctionbyimprovingangiogenicfunctionofepcs AT qiyuan exosomesfromsirt1overexpressingadscsrestorecardiacfunctionbyimprovingangiogenicfunctionofepcs AT zhangwei exosomesfromsirt1overexpressingadscsrestorecardiacfunctionbyimprovingangiogenicfunctionofepcs AT zhangchenjun exosomesfromsirt1overexpressingadscsrestorecardiacfunctionbyimprovingangiogenicfunctionofepcs AT jiangmei exosomesfromsirt1overexpressingadscsrestorecardiacfunctionbyimprovingangiogenicfunctionofepcs AT dengshengqiong exosomesfromsirt1overexpressingadscsrestorecardiacfunctionbyimprovingangiogenicfunctionofepcs AT wanghairong exosomesfromsirt1overexpressingadscsrestorecardiacfunctionbyimprovingangiogenicfunctionofepcs |