Human Bone Marrow Mesenchymal Stem Cells Promote the M2 Phenotype in Macrophages Derived from STEMI Patients

• Published in: International journal of molecular sciences Vol. 24; no. 22; p. 16257
• Main Authors: Cortés-Morales, Víctor Adrián, Vázquez-González, Wendy Guadalupe, Montesinos, Juan José, Moreno-Ruíz, Luis, Salgado-Pastor, Selene, Salinas-Arreola, Pamela Michelle, Díaz-Duarte, Karla, Chávez-Rueda, Adriana Karina, Chávez-Sánchez, Luis
• Format: Journal Article
• Language: English
• Published: Basel MDPI AG 01-11-2023
• Subjects: acute ST-elevation myocardial infarction; Analysis; Bone marrow; bone marrow mesenchymal stem/stromal cells; Cardiovascular disease; Clopidogrel; Coronary vessels; Cytokines; Ethylenediaminetetraacetic acid; Extracellular matrix; Genetic aspects; Genotype & phenotype; Heart attack; Heart attacks; Inflammation; M1 macrophages; M2 macrophages; Macrophages; Myocarditis; regulatory T-cells; Stem cells; T cells; Mexico
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms242216257

Acute ST-elevation myocardial infarction (STEMI) leads to myocardial injury or necrosis, and M1 macrophages play an important role in the inflammatory response. Bone marrow mesenchymal stem/stromal cells (BM-MSCs) are capable of modulating macrophage plasticity, principally due to their immunoregulatory capacity. In the present study, we analyzed the capacity of MSCs to modulate macrophages derived from monocytes from patients with STEMI. We analyzed the circulating levels of cytokines associated with M1 and M2 macrophages in patients with STEMI, and the levels of cytokines associated with M1 macrophages were significantly higher in patients with STEMI than in controls. BM-MSCs facilitate the generation of M1 and M2 macrophages. M1 macrophages cocultured with MSCs did not have decreased M1 marker expression, but these macrophages had an increased expression of markers of the M2 macrophage phenotype (CD14, CD163 and CD206) and IL-10 and IL-1Ra signaling-induced regulatory T cells (Tregs). M2 macrophages from patients with STEMI had an increased expression of M2 phenotypic markers in coculture with BM-MSCs, as well as an increased secretion of anti-inflammatory cytokines and an increased generation of Tregs. The findings in this study indicate that BM-MSCs have the ability to modulate the M1 macrophage response, which could improve cardiac tissue damage in patients with STEMI.