A new role for microRNA-9 in human neural progenitor cells.

Cell cycle (Georgetown, Tex.) (Impact Factor: 5.01). 08/2010; 9(15):2913-4.
Source: PubMed
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    ABSTRACT: The understanding of the events that are responsible for a disease are mandatory for setting up a therapeutic strategy. Although spinal muscular atrophy (SMA) is considered a rare neurodegenerative pathology, its impact in our society is really devastating as it strikes young people from birth onwards, and it affects their families either emotionally or financially. Moreover, it requires intensive care for the children, and this diverts both parents and relatives from their occupations. Each neuron is very different from one other, therefore in a neurodegenerative disease the population of axons, synapses and cell bodies degenerate asynchronously, and subpopulations of neurons have different vulnerabilities. The knowledge of the sequence of events along the lengths of individual neurons is crucial to understand if each synapse degenerates before the corresponding axon, or if each axon degenerates before the corresponding cell body. Early degeneration of one neuronal compartment in disease often reflects molecular defects somewhere else. Up to today SMA is considered mostly a lower motor neuron disease due to the loss-of-function mutations in the SMN1 gene; here we inspect other features that can be altered by this defect such as the cross talk between muscle and motor neuron and the role of physical inactivity.
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    ABSTRACT: The purpose of this study was to investigate the functions of microRNA-9, which is a tissue-specific microRNA in central nervous system, in the vasculogenic mimicry (VM) of glioma cell lines in vitro and in vivo.Glioma cell lines U87MG, U251 and SHG44 were transfected with microRNA-9 mimic, microRNA-9 inhibitor or scramble sequences. The amount of microRNA-9 and Stathmin (STMN1) mRNA was determined by quantitative real-time PCR, and the protein expression of STMN1 was determined by western blot. Cell proliferation and apoptosis were assessed. The interactions between the 3'UTR of STMN1 and miR-9 was determined by luciferase reporter assay. The VM capacity in vitro was evaluated using VM formation assay, and the rescue experiment of STMN1 was carried out in U251 cells. The in vivo experiment was applied with animal models implanted with U87MG cells.MicroRNA-9 mimic transfection reduced proliferation and increased apoptosis in glioma cell lines (p < 0.05). MicroRNA-9 mimic up-regulated STMN1 mRNA levels but reduced its protein levels (p < 0.05), and luciferase activity of STMN1 was suppressed by microRNA-9 mimic transfection (p < 0.05). Furthermore, microRNA-9 mimic transfection suppressed tumor volume growth, as well as VM both in vitro and in vivo. The cell viability and microtube density were upregulated in U251 cells after STMN1 up-regulation (p < 0.05). STMN1 is a target of microRNA-9, and microRNA-9 could modulate cell proliferation, VM and tumor volume growth through controlling STMN1 expression. MicroRNA-9 and its targets may represent a novel panel of molecules for the development of glioma treatment.
    Journal of Neuro-Oncology 09/2013; DOI:10.1007/s11060-013-1245-9 · 2.79 Impact Factor
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    ABSTRACT: Developmental studies and experimental data have enabled us to assert that the terminal cell differentiation state is reversible, and that altering the balance of specific transcription factors could be a powerful strategy for inducing pluripotency. Due to the risks related to using induced pluripotent cells in clinical applications, biologists are now striving to develop methods to induce a committed differentiated cell type by direct conversion of another cell line. Several reprogramming factors have been discovered, and some cellular phenotypes have been obtained by novel transdifferentiation processes. It has been recently demonstrated that induced neural stem cells (iNSCs) can be obtained from rodent and human somatic cells, like fibroblasts, through the forced expression of defined transcription factors. To date, two different approaches have been successfully used to obtain iNSCs: a direct method and an indirect method that involves an intermediate destabilized state. The possibility to induce characterised iNSCs from human cells, e.g. fibroblasts, has opened new horizons for research in human disease modelling and cellular therapeutic applications in the neurological field. This review focuses on reported reprogramming techniques and innovative techniques that can be further explored in this area, as well as on the criteria for the phenotypic characterization of iNSCs and their use in developing novel therapeutic strategies for neurological diseases.
    Progress in Neurobiology 11/2013; 114. DOI:10.1016/j.pneurobio.2013.11.001 · 10.30 Impact Factor

Celine Delaloy