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    • Attempts to expand olfactory stem cells

    2018-11-12

    Attempts to expand olfactory stem mth1 inhibitor according to the free-floating cell aggregate central nervous system (CNS) neurosphere culture method (Reynolds and Weiss, 1992) have been described (Barraud et al., 2007; Sicard et al., 1998; Carter et al., 2004). Olfactory spheres (OSs), clusters of cells generated by culturing the olfactory mucosa, contain cells expressing markers of neural stem cells, glial cells, and neural cells (Murrell et al., 2005; Othman et al., 2005; Murdoch and Roskams, 2008; Tome et al., 2009; Krolewski et al., 2011), but little is known about the properties of OS cells. For example, rat embryonic olfactory mucosa generates 2 distinct types of spherical cell clusters (Tome et al., 2009). One type contains multipotential cells with mesenchymal stem cell-like characteristics and originates in the lamina propria. The second cell type of spherical cell clusters displays epithelial cell characteristics and originates in the olfactory epithelium. Barraud et al. also used OS culture to expand neonatal olfactory mucosa-derived progenitor cells (Barraud et al., 2007).
    Materials and methods
    Results
    Discussion
    Conclusions
    Conflict of interest
    Acknowledgments This study was supported by a Grant-in-Aid for Young Scientists (B), Grant-in-Aid for Scientific Research (C) and the Funding Program for World-Leading Innovative R&D on Science and Technology. We thank Y. Tsujimoto for the generous provision of laboratory equipment. We thank H. Yamazaki for the technical help with FACS analyses, N. Oda for the OS culture, and Y. Takahashi for the administrative assistance.
    Introduction Thyroid hormones have, beside their wide-spread influences on cell metabolism, profound effects on growth and embryonic and postnatal developments. Hypothyroidism before birth or in early childhood induces neurological defects like mental retardation, cerebral spastic diplegia and deaf–mutism (Williams, 2008; Porterfield and Hendrich, 1993). Abnormal hormone levels influence migration, proliferation and differentiation of various neural cell types especially in the central nervous system (Nunez et al., 2008; Horn and Heuer, 2010; Lemkine et al., 2005; Konig and Moura, 2002). The various observed effects depend on cell type, localization, cell function, and hormone level (Chen et al., 2011; Puzianowska-Kuznicka et al., 2006). Most of the effects of thyroid hormones are mediated through thyroid hormone receptors (TR) that act as ligand dependent transcription factors. TRs are products of two genes, THRA and THRB. Four different splice variants of these genes, termed Trα1, Trα2, Trβ1, and Trβ2 have been described of which only three, Trα1, Trβ1, and Trβ2 are able to bind thyroid hormones (Yen, 2001). TRs are present in nearly every mammalian tissue but show remarkable differences in their expression levels. Trα and Trβ1 receptors appear in nearly every part of the body and represent the main receptors in neural tissues, whereas Trβ2 is located mainly in the pituitary gland (Hodin et al., 1989; Bradley et al., 1992). Although thyroid hormone receptors are well studied, many of their target genes are still unknown. Apart from the transcriptional regulation mediated by the thyroid hormone receptors, non-TR-mediated effects have been described (Leonard, 2008; Davis and Davis, 1996). The ENS is a complex autonomous neural network that is mostly divided into two plexus: The myenteric plexus is located between the circular and longitudinal muscle layers forming the tunica muscularis, and the submucosal plexus is located in the tela submucosa of the intestinal wall (Gershon, 1981; Schemann and Neunlist, 2004). Both neural structures coordinate bowel motility, blood flow and secretion of the gut and are also involved in immune defense reactions (Gershon, 1999; Benarroch, 2007). The ENS derives from neural crest cells that migrate from the early developing neural tube into and along the gut. These cells differentiate into a vast number of neural cell types and form a complex neural network (Burns and Thapar, 2006; Gershon et al., 1993; Anderson et al., 2006; Burns, 2005). Perturbation of migration, proliferation or differentiation of enteric neural crest cells leads to congenital defects of the ENS like the Hirschsprung disease (HSCR) that occurs in about 1 of 5000 human newborns. HSCR is characterized by a complete lack of neurons from variable lengths of the colon and is associated with life-threatening dysregulation of propulsive bowel motility (Amiel et al., 2008). An appropriate therapy for enteric disorders might include ENS neural stem and progenitor cells (Heanue and Pachnis, 2007). These cells have already been isolated from fetal, postnatal and adult murine and from fetal and early postnatal human gut (Metzger et al., 2009; Bondurand et al., 2003). They can be expanded in cell culture and are able to differentiate into various cells like neuronal and glial cell types. Thus, they are an ideal cell pool for studies comprising mechanisms and factors that are involved in the development and cell biological function of the ENS.