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Showing papers on "Mesoangioblast published in 2017"


Journal ArticleDOI
TL;DR: It is demonstrated that membrane vesicles released by mesoangioblasts contain Hsp70, and that the released HSp70 is able to interact by an autocrine mechanism with Toll‐like receptor 4 (TLR4) and CD91 to stimulate migration and present a paradigm shift in the understanding of the molecular mechanisms that regulate mesOangioblast stem cells ability to traverse the extracellular matrix (ECM).
Abstract: Mouse mesoangioblasts are vessel-associated progenitor stem cells endowed with the ability of multipotent mesoderm differentiation. Therefore, they represent a promising tool in the regeneration of injured tissues. Several studies have demonstrated that homing of mesoangioblasts into blood and injured tissues are mainly controlled by cytokines/chemokines and other inflammatory factors. However, little is known about the molecular mechanisms regulating their ability to traverse the extracellular matrix (ECM). Here, we demonstrate that membrane vesicles released by mesoangioblasts contain Hsp70, and that the released Hsp70 is able to interact by an autocrine mechanism with Toll-like receptor 4 (TLR4) and CD91 to stimulate migration. We further demonstrate that Hsp70 has a positive role in regulating matrix metalloproteinase 2 (MMP2) and MMP9 expression and that MMP2 has a more pronounced effect on cell migration, as compared to MMP9. In addition, the analysis of the intracellular pathways implicated in Hsp70 regulated signal transduction showed the involvement of both PI3K/AKT and NF-κB. Taken together, our findings present a paradigm shift in our understanding of the molecular mechanisms that regulate mesoangioblast stem cells ability to traverse the extracellular matrix (ECM). J. Cell. Physiol. 232: 1845-1861, 2017. © 2016 Wiley Periodicals, Inc.

17 citations


Journal ArticleDOI
TL;DR: Taken together, the results candidate Magic-F1 as a potent myogenic inducer, able to affect positively the vascular network, increasing vessel number in fast twitch fibers and modulating the gene expression profile in myogenic progenitors.
Abstract: Met-Activating Genetically Improved Chimeric Factor-1 (Magic-F1) is an engineered protein that contains two human Met-binding domains. Previous experiments in both homozygous and hemizygous transgenic mice demonstrated that the skeletal muscle specific expression of Magic-F1 can induce a constitutive muscular hypertrophy, increasing the vessel number in fast twitch fibers, also improving running performance and accelerating muscle regeneration after injury [1]. We also found that Magic-F1 could be responsible of muscular hypertrophy inteacting with Pax3 signal pathway in skeletal muscle precursor cells [2]. In order to evaluate the therapeutic potential of Magic-F1, we tested its effect on multipotent and pluripotent stem cells [3]. Murine mesoangioblasts (adult vessel-associated stem cells) expressing Magic-F1 were able to differentiate spontaneously forming myotubes. In addition, in Magic-F1 inducible murine embryonic stem cells subjected to myogenic differentiation, the presence of recombinant protein resulted in improved myogenic commitment. Finally, the microarray analysis of Magic-F1+/+ satellite cells evidenced transcriptomic changes in genes involved in the control of muscle growth, development and vascularisation [4]. Taken together our results candidate Magic-F1 as a potent myogenic inducer, able to affect positively the vascular network, increasing vessel number in fast twitch fibers and modulating the gene expression profile in myogenic progenitors.