1,721,019 research outputs found
Exon-skipping of dysferlin in CD133+ stem cells isolated from normal and patient affected with dysferlinopathies
No full textMicroRNA-206 is Upregulated in an Animal Model of Duchenne Muscular Dystrophy
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Cell Based Therapy for Duchenne Muscular Dystrophy
No full textMutations in the dystrophin gene cause an X-linked genetic disorder: Duchenne muscular dystrophy (DMD). Stem cell therapy is an attractive method to treat DMD because a small number of cells are required to obtain a therapeutic effect. Here, we discussed about multiple types of myogenic stem cells and their possible use to treat DMD. The identification of a stem cell population providing efficient muscle regeneration is critical for the progression of cell therapy for DMD. We speculated that the most promising possibility for the treatment of DMD is a combination of different approaches, such as gene and stem cell therapy
Stem Cell Tracking by Nanotechnologies
No full textAdvances in stem cell research have provided important understanding of the cell biology and offered great promise for developing new strategies for tissue regeneration. The beneficial effects of stem cell therapy depend also by the development of new approachs for the track of stem cells in living subjects over time after transplantation. Recent developments in the use of nanotechnologies have contributed to advance of the high-resolution in vivo imaging methods, including positron emission tomography (PET), single-photon emission tomography (SPECT), magnetic resonance (MR) imaging, and X-Ray computed microtomography (microCT). This review examines the use of nanotechnologies for stem cell tracking
Development of New technologies Inducing Myogenic Differentiation of Human Circulating CD133+ Cells
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Identification of miRNAs to improve myogenic differentiation of Mesenchymal Stem Cells as regenerative therapy for Duchenne muscular dystrophy
No full textDuchenne muscular dystrophy (DMD) is a recessive X-linked form of muscular dystrophy caused by mutations in the dystrophin gene. The absence of the protein caused fibrotic tissue deposition and adipose infiltration into the muscle until complete replacement of original tissue at later stages of the disease and DMD patients die from heart and respiratory failure. Unravelling the precise cellular origin and molecular mechanism of fibrotic and adipogenic tissue within a degenerating human DMD muscle is crucial to understand if the dystrophic muscle environment could influence the outcome of stem cells based therapy and to improve future treatments. Recently, we isolated through FACS sorting from dissociated muscular biopsies two MSC populations that express or not the CD133 antigen. These populations could be responsible for muscle regeneration exhaustion and adipogenic tissue deposition in DMD. We identified miRNAs involved in in-vitro differentiation process and in DMD muscle degeneration in the isolated CD133+ and CD133- hmMSCs and unravelled gene regulatory networks that miRNAs control in DMD. In a clinical prospective, we also tested the therapeutic value of targeting miRNAs to enhance transduction efficiency of hmMSCs into muscle using a dystrophic animal model (scid-mdx mice)
Difference in Myogenic properties of the human blood-derived stem cells subpopulation isolated from normal and dystrophic tissues
No full textMesenchymal and myogenic precursor cells : old partners for few interactions
No full textIn adult tissues, somatic stem cells represent a cell reservoir involved in physiological or pathological cell replacement. In several myopathies, chronic inflammation causes fibrotic infiltrations and adipose deposition within degenerating tissue. Starting from this evidence, we developed an experimental model for mimicking in vitro the effects of a damaged muscle on a specific stem cell population; the method is based on the simultaneous culture of stem cells and muscle tissue sections, in a microenvironment divided by a porous membrane, that guarantees soluble factors exchange but not cell migration. Human blood and adipose derived stem cells were grown in presence of normal (C57BL mouse) or dystrophic (mdx mouse model) muscle sections. Blood derived stem cells, co-cultured with muscle sections, showed an increase in cell proliferation and expression of mesenchymal markers, such as CD105, CD44, CD90, CD73 and CD29; moreover, they were able to express early myogenic differentiation markers, such as Myf5. Instead, human adipose derived stem cells showed an opposite behaviour; cells cultured in presence of both normal and dystrophic muscle tissue sections displayed an adipogenic differentiation. Moreover, the number of cells derived from the adipose mesenchymal stem cells and expressing Oil Red O lipid vacuole, Perilipin A and FABP4 was higher in the presence of dystrophic than normal muscle sections. These data suggest that the factors released by degenerating dystrophic muscle tissue may determine the commitment of mesenchymal stem cells into an adipogenic lineage underlying a new paradigm of the role of mesenchymal stem cells in the adipose formation of dystrophic muscle tissu
Proliferation and clonal Characterization of Human Muscle Derived CD133+ Stem Cell Define an Intrinsic Heterogeneity
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