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In another setting, a male mouse model for high running performance recruited myogenic precursor cells/SATCs with lower activation thresholds that responded more rapidly to external stimuli and were more primed for differentiation at the expense of more primitive cells. Recently, various strategies using a hydrogel-based system, both as encapsulated stem cells and as biocompatible patches loaded with stem cells and applied at the tissue damage site, were developed for regenerating the infarcted myocardium [[14]]. Embryonic and induced pluripotent stem cells (ESCs and iPSCs), as well as adult stem cells, hold great promise for future cell replacement therapies. Growing evidence indicates that some of the observed therapeutic outcomes of stem cell-based therapy are due to paracrine effects (including extracellular vesicles), rather than long-term engraftment or the survival of transplanted cells [[1]]. [Extracted from the article]

Background: Acute myeloid leukemia (AML) is a hematopoietic malignancy in which antitumor immunity is impaired. The therapeutic management of AML requires understanding the mechanisms involved in the fragility and immune dysfunction of AML T lymphocytes. Methods: In this study, T lymphocytes from healthy donors (HD) and AML patients were used. Extracellular vesicles (EVs) from leukemic cells were screened for their microRNA content and impact on T lymphocytes. Flow cytometry, transcriptomic as well as lentiviral transduction techniques were used to carry out the research. Results: We observed increased cell death of T lymphocytes from AML patients. EVs from leukemia myeloid cell lines harbored several miRNAs, including miR-21, and were able to induce T lymphocyte death. Compared to that in HD, miR-21 was overexpressed in both the bone marrow fluid and infiltrating T lymphocytes of AML patients. MiR-21 induces T lymphocyte cell death by upregulating proapoptotic gene expression. It also increases the immunosuppressive profile of T lymphocytes by upregulating the IL13, IL4, IL10, and FoxP3 genes. Conclusions: Our results demonstrate that miR-21 plays a significant role in AML T lymphocyte dysfunction and apoptosis. Targeting miR-21 may be a novel approach to restore the efficacy of the immune response against AML. [ABSTRACT FROM AUTHOR]