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    • Interestingly the migration kinetics of

    2018-10-20

    Interestingly, the migration kinetics of type B astrocytes was similar to that previously described for neuroblasts (Elvira et al., 2012). This suggests that both cell types are able to respond to the same “damage signals” and that type B astrocytes could help in neuroblast migration as previously suggested from in vitro (Song et al., 2002; Lim and Alvarez-Buylla, 1999) or in vivo data (Kriegstein and Alvarez-Buylla, 2009; Leavitt et al., 1999; Noctor et al., 2001; Alvarez-Buylla and Nottebohm, 1988). Nilo1+ radial glia-like processes reported here support the notion that radial glia is a mainstay for neurogenesis not only during the embryonic stage but also during adulthood. The migration of neural stem cells reported here is fully in accordance with data showing that stimulation with exogenous growth factors increase cell proliferation at the SVZ and promote the migration of SVZ-derived cells into the adjacent parenchyma or even at the vicinity of a brain lesion site (Cantarella et al., 2008; Teramoto et al., 2003; Craig et al., 1996; Doetsch et al., 2002; Gonzalez-Perez et al., 2009). Growth factor infusions also increased the number of GFAP+ cells exhibiting long processes that link the ischemic striatum to the SVZ niche (Teramoto et al., 2003). The lesion it self induces the secretion of growth and trophic factors (Sundholm-Peters et al., 2005; Goings et al., 2004; Ridet et al., 1997; Suzuki et al., 2012) that could activate quiescent precursors (Ridet et al., 1997) or modify astrocyte morphology (Junier, 2000) resulting in the mobilization SVZ-derived cells.
    Conclusions In summary, our data show that by combining Nilo1, a monoclonal antibody able to identify surface buy GSK1324726A in type B astrocytes and radial glia during development, with superparamagnetic nanoparticles, the adult neural stem cells can be identified in their niches and follow their fast and orderly migration towards a lesion site in vivo using MRI. Furthermore, the migration of these cells towards a lesion site seems to be a general trait, since it can be detected during development of a tumor, following a cryolesion, demyelination or even a mechanical injury, generating in addition few hours after the damage radial glia-like structures at the lesion site. The following are the supplementary data related to this article.
    Acknowledgments This work was supported by grants from the Instituto de Salud Carlos III (grant RD06/0010/1010 to JAGS), and the Ministry of Science and Innovation (grants SAF2009-07974 to JAGS, CTQ-2011-271268 to SP, AMIT, CENIT-CDTI to MD). We would like to thank Prof. T.N. Syfried, Boston, MA, USA and Dr. A. Martinez (I. Cajal, Madrid, Spain) for providing CT-2A and GFP-CT-2A cells respectively. Dr. L. Kremer (ProteinTools, CNB-CSIC, Madrid, Spain) for help and advice on mAb purification and labeling. We are grateful to M.T. Seisdedos and to the CIB animal and confocal microscopy facilities.
    Introduction Induced neural stem cells (iNSCs) are reprogrammed cells that possess features like bona fide neural stem cells (NSCs). In 2012, we have reported that mouse somatic cells—sertoli cells, can be directly converted to iNSCs by introduction of 8 transcription factors (Sheng et al., 2012a), which provides further evidence that somatic cells can be induced to not only pluripotent stem cells (PSCs) (Takahashi and Yamanaka, 2006; Takahashi et al., 2007; Yu et al., 2007), mature neurons (Vierbuchen et al., 2010; Pfisterer et al., 2011; Caiazzo et al., 2011; Kim et al., 2011), but also to adult stem cells. The above findings support the concept that the fates of any two different lineages are interchangeable, given sufficient and necessary conditions. Lmx1a is a key determinant in the specification of dopaminergic (DA) neurons (Deng et al., 2011; Andersson et al., 2006). When exogenously expressed in embryonic stem (ES) cells, LMX1a markedly enhances the efficiency for DA neuron production (Friling et al., 2009). We thus speculate that expression of Lmx1a in iNSCs may further increase their capacity to differentiate to DA neurons. In this study, we aim to investigate whether iNSCs are safe and/or efficacious in a mouse PD model, and whether expression of Lmx1a in iNSCs can further enhance the therapeutic efficacy.