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Bone marrow-derived mesenchymal stem cells attenuate myocardial ischemia–reperfusion injury via upregulation of splenic regulatory T cells

BACKGROUND: Myocardial ischemia–reperfusion injury (MIRI) is the main pathological manifestation of cardiovascular diseases such as myocardial infarction. The potential therapeutic effects of bone marrow-derived mesenchymal stem cells (BM-MSCs) and the participation of regulatory T cells (Tregs) in...

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Detalles Bibliográficos
Autores principales: Pang, Ling-Xiao, Cai, Wen-Wei, Li, Qian, Li, Heng-Jie, Fei, Min, Yuan, Yong-Sheng, Sheng, Bin, Zhang, Ke, An, Rong-Cheng, Ou, Ying-Wei, Zeng, Wen-Jie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8080373/
https://www.ncbi.nlm.nih.gov/pubmed/33906602
http://dx.doi.org/10.1186/s12872-021-02007-4
Descripción
Sumario:BACKGROUND: Myocardial ischemia–reperfusion injury (MIRI) is the main pathological manifestation of cardiovascular diseases such as myocardial infarction. The potential therapeutic effects of bone marrow-derived mesenchymal stem cells (BM-MSCs) and the participation of regulatory T cells (Tregs) in MIRI remains to be defined. METHODS: We used the experimental acute MIRI that was induced in mice by left ascending coronary ischemia, which were subsequently randomized to receive immunoglobulin G (IgG) or anti-CD25 antibody PC61 with or without intravenously injected BM-MSCs. The splenectomized mice underwent prior to experimental MIRI followed by intravenous administration of BM-MSCs. At 72 h post-MIRI, the hearts and spleens were harvested and subjected to cytometric and histologic analyses. RESULTS: CD25(+)Foxp3(+) regulatory T cells were significantly elevated after MIRI in the hearts and spleens of mice receiving IgG + BM-MSCs and PC61 + BM-MSCs compared to the respective control mice (all p < 0.01). This was accompanied by upregulation of interleukin 10 and transforming growth factor β1 and downregulation of creatinine kinase and lactate dehydrogenase in the serum. The post-MIRI mice receiving BM-MSCs showed attenuated inflammation and cellular apoptosis in the heart. Meanwhile, splenectomy compromised all therapeutic effects of BM-MSCs. CONCLUSION: Administration of BM-MSCs effectively alleviates MIRI in mice through inducing Treg activation, particularly in the spleen. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12872-021-02007-4.