Microvesicles secreted from equine amniotic-derived cells and their potential role in reducing inflammation in endometrial cells in an in-vitro model
It is known that a paracrine mechanism exists between mesenchymal stem cells and target cells. This process may involve microvesicles (MVs) as an integral component of cell-to-cell communication. In this context, this study aims to understand the efficacy of MVs in in-vitro endometrial stressed cell...
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Veröffentlicht in: | Stem cell research & therapy 2016-11, Vol.7 (1), p.169-169, Article 169 |
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Sprache: | eng |
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Zusammenfassung: | It is known that a paracrine mechanism exists between mesenchymal stem cells and target cells. This process may involve microvesicles (MVs) as an integral component of cell-to-cell communication.
In this context, this study aims to understand the efficacy of MVs in in-vitro endometrial stressed cells in view of potential healing in in-vivo studies. For this purpose, the presence and type of MVs secreted by amniotic mesenchymal stem cells (AMCs) were investigated and the response of endometrial cells to MVs was studied using a dose-response curve at different concentrations and times. Moreover, the ability of MVs to counteract the in vitro stress in endometrial cells induced by lipopolysaccharide was studied by measuring the rate of apoptosis and cell proliferation, the expression of some pro-inflammatory genes such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin 1β (IL-1β), and metalloproteinases (MMP) 1 and 13, and the release of some pro- or anti-inflammatory cytokines.
MVs secreted by the AMCs ranged in size from 100 to 200 nm. The incorporation of MVs was gradual over time and peaked at 72 h. MVs reduced the apoptosis rate, increased cell proliferation values, downregulated pro-inflammatory gene expression, and decreased the secretion of pro-inflammatory cytokines.
Our data suggest that some microRNAs could contribute to counteracting in-vivo inflammation of endometrial tissue. |
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ISSN: | 1757-6512 1757-6512 |
DOI: | 10.1186/s13287-016-0429-6 |