Human Adipose-derived mesenchymal stem cells promote lymphocyte apoptosis and alleviate atherosclerosis via miR-125b-1-3p/BCL11B signal axis.
Yu C., Tang W., Lu R., Tao Y., Ren T., Gao Y.
Animal Study, published in Ann Palliat Med (2021) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Ann Palliat Med (2021)
- Country
- China
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 33725769
- DOI
- 10.21037/apm-21-49
- Citations
- 17
Abstract (original English)
Background Mesenchymal stem cells (MSCs) have shown great potential in the treatment of cardiovascular diseases, with fat being a more accessible source of MSCs. This study investigated the effect of human adipose-derived mesenchymal stem cells (hMSCs-Ad) exosomes on T lymphocytes and its role in atherosclerosis (AS). Methods The exosomes were preliminarily isolated hMSCs-Ad and co-cultured with human H9 T lymphocytes. The effects of hMSCs-Ad exosomes on the proliferation and apoptosis of H9 were examined by performing functional experiments. The serum lipid level and inflammatory factor level in tail vein of mice were measured by biochemical analyzer and enzyme linked immunosorbent assay (ELISA) respectively. Results The hMSCs-Ad-derived exosomes up-regulate the expression of micro (mi)R-125b-1-3p in H9 and AS arterial tissues. miR-125b-1-3p shared a targeted binding site with B-cell chronic lymphocytic leukemia (CLL)/lymphoma 11B gene (BCL11B). miR-125b-1-3p negatively regulated the expression of BCL11B in H9, and that knocking down BCL11B in H9 promoted its apoptosis. Injection of hMSCs-Ad-derived exosomes via the tail vein effectively reduced blood lipid and inflammatory factors, and that relieved the symptoms of AS in AS model mice. Conclusions miR-125b-1-3p was expressed in hMSCs-Ad exosomes and can promote T lymphocyte apoptosis and alleviate AS by down-regulating BCL11B
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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