Mesenchymal Stem Cells Pretreatment With Stromal-Derived Factor-1 Alpha Augments Cardiac Function and Angiogenesis in Infarcted Myocardium.


Journal

The American journal of the medical sciences
ISSN: 1538-2990
Titre abrégé: Am J Med Sci
Pays: United States
ID NLM: 0370506

Informations de publication

Date de publication:
06 2021
Historique:
received: 05 05 2020
revised: 15 12 2020
accepted: 26 01 2021
pubmed: 15 2 2021
medline: 21 7 2021
entrez: 14 2 2021
Statut: ppublish

Résumé

Stem cell therapy is among the novel approaches for the treatment of post-myocardial infarction cardiomyopathy. This study aims to compare the effect of stromal-derived factor 1 α (SDF1α), mesenchymal stem cells (MSCs) in combination with the lentiviral production of vascular endothelial growth factor (VEGF) on infarct area, vascularization and eventually cardiac function in a rat model of myocardial infarction (MI). The influence of SDf1α on MSCs survival was investigated. MSCs were transduced via a lentiviral vector containing VEGF. After that, the effect of mesenchymal stem cell transfection of VEGF-A165 and SDf1α preconditioning on cardiac function and scar size was investigated in five groups of MI rat models. The MSC survival, cardiac function, scar size, angiogenesis, and lymphocyte count were assessed 72 hours and 6 weeks after cell transplantation. SDF1α decreased the lactate dehydrogenase release in MSCs significantly. Also, the number of viable cells in the SDF1α-pretreated group was meaningfully more than the control. The left ventricular systolic function significantly enhanced in groups with These findings suggest that SDF1α pretreatment and overexpressing VEGF in MSCs could augment the MSCs' survival in the infarcted myocardium, reduce the scar size, and improve the cardiac systolic function.

Sections du résumé

BACKGROUND
Stem cell therapy is among the novel approaches for the treatment of post-myocardial infarction cardiomyopathy. This study aims to compare the effect of stromal-derived factor 1 α (SDF1α), mesenchymal stem cells (MSCs) in combination with the lentiviral production of vascular endothelial growth factor (VEGF) on infarct area, vascularization and eventually cardiac function in a rat model of myocardial infarction (MI).
METHODS
The influence of SDf1α on MSCs survival was investigated. MSCs were transduced via a lentiviral vector containing VEGF. After that, the effect of mesenchymal stem cell transfection of VEGF-A165 and SDf1α preconditioning on cardiac function and scar size was investigated in five groups of MI rat models. The MSC survival, cardiac function, scar size, angiogenesis, and lymphocyte count were assessed 72 hours and 6 weeks after cell transplantation.
RESULTS
SDF1α decreased the lactate dehydrogenase release in MSCs significantly. Also, the number of viable cells in the SDF1α-pretreated group was meaningfully more than the control. The left ventricular systolic function significantly enhanced in groups with
CONCLUSIONS
These findings suggest that SDF1α pretreatment and overexpressing VEGF in MSCs could augment the MSCs' survival in the infarcted myocardium, reduce the scar size, and improve the cardiac systolic function.

Identifiants

pubmed: 33582157
pii: S0002-9629(21)00054-9
doi: 10.1016/j.amjms.2021.01.025
pii:
doi:

Substances chimiques

CXCL12 protein, rat 0
Chemokine CXCL12 0
Recombinant Proteins 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

765-775

Informations de copyright

Copyright © 2021 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.

Auteurs

Rezvan Esmaeili (R)

Genetics Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR, Tehran, Iran; Department of Genetics, School of Biological Sciences, Tarbiat Modares University, Tehran, Iran.

Amir Darbandi-Azar (A)

Rajaie Cardiovascular Medical and Research Centre, Iran University of Medical Sciences, Tehran, Iran.

Anita Sadeghpour (A)

Echocardiography Research Center, Department of Cardiovascular Medicine, Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran.

Keivan Majidzadeh-A (K)

Genetics Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR, Tehran, Iran; Tasnim Biotechnology Research Center (TBRC), Faculty of Medicine, AJA University of Medical Sciences, Tehran, Iran. Electronic address: kmajidzadeh@acecr.ac.ir.

Leila Eini (L)

Cell and Immunotherapy Department, Breast Cancer Research Center, Motamed Cancer Institute ACECR, Tehran, Iran.

Narges Jafarbeik-Iravani (N)

Genetics Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR, Tehran, Iran.

Parisa Hoseinpour (P)

Breast Cancer Research Center, Motamed Cancer Institute, ACECR, Tehran, Iran.

Alireza Vajhi (A)

Department of Surgery and Radiology, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran.

Tayebeh Oghabi Bakhshaiesh (T)

Genetics Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR, Tehran, Iran.

Farzad Masoudkabir (F)

Cardiac Primary Prevention Research Center, Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran.

Majid Sadeghizadeh (M)

Department of Genetics, School of Biological Sciences, Tarbiat Modares University, Tehran, Iran. Electronic address: sadeghma@modares.ac.ir.

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Classifications MeSH