Introduction: Mouse mesoangioblasts are vessel-associated multipotentprogenitor stem cells, which are able to differentiate intodifferent mesodermal cell types. In our previous paper, we havedemonstrated that mesoangioblasts are able to shed in the extracellularenvironment membrane vesicles (EVs), which contain bothstructural proteins and biological factors such as FGF2 and the twogelatinases MMP2/9. We investigated whether these EV interact in aparacrine way with other cell types different from mesoangioblasts,and eventually the effects of this interaction. Methods: MesoangioblastEVs were collected from conditioned media by ultracentrifugation.Total mRNAs from mesoangioblasts and from two preparations of EVs were used to perform microarray. Different concentrations ofmesoangioblast EV were used to evaluate in vitro migration modulationon human ECV304 cells by wound healing assay or study theirinfluence on capillary-like structures formation. Murine RAW 264.7macrophages were cultured with or without mesoangioblast-derivedEVs to investigate their effect on cytokines secretion profile and RTKphosphorylation levels by array. Results: We observed that mesoangioblastEV contained a huge amount of mRNA; most of thetranscripts are co-expressed in EV and cells, whereas 20 mRNA wereaccumulated within EV and absent in the cells. Gene ontologyanalysis showed that the common mRNA could be involved in cellsurvival and differentiation. We demonstrated that mesoangioblastEV interact with endothelial ECV304 cells by positively influencingtheir migration capability. Moreover, they induce in vitro the ECV304differentiation versus capillary-like structures depending on theirconcentration. Mesoangioblast EVs are also able to interact with RAW264.7 cells inducing dramatic changes in cytokines secretion and inRTK phosphorylation levels. Conclusions: We demonstrated thatmesoangioblast EV interact with endothelial cells and macrophagesand influence on their behaviour.
|Number of pages||1|
|Journal||Journal of Extracellular Vesicles|
|Publication status||Published - 2016|