Human Placental Mesenchymal Stem/Stromal cells (pMSCs) inhibit agonist-induced platelet functions reducing atherosclerosis and thrombosis phenotypes
Al Subayyil A., Basmaeil YS., Alenzi R., Khatlani T.
Prospective Study, published in J Cell Mol Med (2021) — summary generated from the PubMed abstract.
Early human evidence such as case series or small samples is exploring possible benefits.
- 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
- Prospective Study
- Journal
- J Cell Mol Med (2021)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 34535958
- PMCID
- PMC8500971
- DOI
- 10.1111/jcmm.16848
- Citations
- 14
Abstract (original English)
Mesenchymal stem/stromal cells isolated from human term placenta (pMSCs) have potential to treat clinically manifested inflammatory diseases. Atherosclerosis is a chronic inflammatory disease, and platelets play a contributory role towards its pathogenesis. During transplantation, MSCs interact with platelets and exert influence on their functional outcome. In this study, we investigated the consequences of interaction between pMSCs and platelets, and its impact on platelet-mediated atherosclerosis in vitro. Human platelets were treated with various types of pMSCs either directly or with their secretome, and their effect on agonist-mediated platelet activation and functional characteristics were evaluated. Human umbilical vein endothelial cells (HUVECs) were used as control. The impact of pMSCs treatment on platelets was evaluated by the expression of activation markers and by platelet functional analysis. A subset of pMSCs reduced agonist-induced activation of platelets, both via direct contact and with secretome treatments. Decrease in platelet activation translated into diminished spreading, limited adhesion and minimized aggregation. In addition, pMSCs decreased oxidized LDL (ox-LDL)-inducedCD36-mediated platelet activation, establishing their protective role in atherosclerosis. Gene expression and protein analysis show that pMSCs express pro- and anti-thrombotic proteins,
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
Evidence level
Early human evidence such as case series or small samples is exploring possible benefits.
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