Project description:To identify specific miRNAs carried by MenSC-EVs, and explore their crucial roles in MenSC-EV-based improvement of inflammatory diseases.
Project description:Mesenchymal stromal cells (MSCs) have been shown to exert their therapeutic effects through the secretion of various paracrine factors, including extracellular vesicles (EVs). These EVs are now being developed as a promising alternative to cell-based therapies. Menstrual blood-derived stromal cells (MenSCs) are a type of MSC that have emerged as a innovative source due to their immunomodulatory and regenerative properties. Additionally, new strategies of cell priming could potentially alter the concentration and cargo of released EVs, leading to modifications in their biological properties. In this study, we aimed to characterize the EVs released by MenSCs and to compare their therapeutic potential under three different preconditioning conditions (proinflammatory stimuli, physioxia, and acute hypoxia).
Project description:To identify specific miRNAs carried by hUCMSC-EVs, and explore their crucial roles in hUCMSC-EV-based improvement of inflammatory diseases.
Project description:CD4+ T cells release extracellular vesicles during their differentiation process. It is known that miRNAs encapsulated within these extracellular vesicles (EVs) are involved in the regulation of cellular function and the control of disease. It has become increasingly clear that secretory PLA2 (sPLA2), an extracellular metabolic enzyme, metabolizes the membrane lipids of EVs and regulates their function. Therefore, we focused on PLA2G12A, a member of the sPLA2 family, and investigated whether its deficiency alters the miRNA profile. We isolated naive T cells from mouse spleens, differentiated them into Th17 cells using a Th17 differentiation culture system, and analyzed the EVs released during this process. Although no significant overall differences were observed between wild-type and gene-deficient, differences in expression levels were confirmed for specific miRNAs. These miRNAs were factors regulating Th17 cell differentiation. These results suggest that PLA2G12A alters the composition of EVs.
Project description:Vascular calcification often occurs with osteoporosis, a contradictory association called “calcification paradox”. We find that extracellular vesicles (EVs) released from aged bone matrix (AB-EVs) during bone resorption favor adipogenesis rather than osteogenesis of BMSCs and augment calcification of vascular smooth muscle cells (VSMCs). Intravenous or intramedullary injection of AB-EVs promotes bone-fat imbalance and exacerbates Vitamin D3 (VD3)-induced vascular calcification in young or old mice. To explore the involvement of miRNAs in the AB-EVs-induced promotion of adipocyte formation and vascular calcification, the Agilent miRNA array was conducted to compare the miRNA expression profiles in AB-EVs and YB-EVs from mouse bone specimens. Our study uncovers the role of AB-EVs as a messenger for calcification paradox by transferring functional miRNAs.
Project description:To investigated dysregulated miRNAs in human MDS patients, we performed miRNA-sequencing (miRNA-seq) of serum EVs from 38 MDS patients and 8 healthy subjects. The miRNA profile in EVs from MDS patients was distinctly clustered from that in healthy individuals. In addition, the miRNAs significantly upregulated in the MDS group target pathways linked to cell survival, proliferation, and MSC differentiation, indicating that they have remarkably similar properties to miRNAs in murine EVs from MDS cells. These results suggest that miRNAs play an essential role in the MSC impairment observed in MDS.