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  • Alternately taurine may be affecting

    2018-10-29

    Alternately, taurine may be affecting the rate of cell migration and through this mechanism accelerate cell proliferation. By increasing cell adhesion or/and accelerating migration on the plate, cells get close faster and this proximity may then generate a propitious condition for proliferation, as has been suggested (Mori et al., 2006). In any event, the time course of the taurine effects on BrdU incorporation suggests its influence on mechanisms related to the progress of the DNA replication phase of the proliferation cell cycle. Taurine might exert this action by directly influencing the chromatin structure, via electrostatic or hydrophobic interactions with the DNA. There is evidence showing the presence of high taurine levels in nuclei of other cell types (Lobo et al., 2000a,b). Thus, taurine could favor a more propitious chromatin configuration for DNA synthesis, and via this action regulate NPC proliferation (Buche et al., 1989). This possibility is now under investigation in our laboratory. The present results in NPCs from the present study may be relevant for the taurine role in kv1.3 inhibitor development. Since the early studies of Sturman et al. (1985), it is known that taurine deficiency impairs brain development, disturbing the sequence of cell mitosis, migration and organization. After three decades, the reason for this taurine requirement for optimal brain development remains obscure. An in vitro system as that used in the present study offers a useful experimental model to clarify the role of taurine on brain developing cells. Taurine may also be required for neurogenesis in the adult brain. One of the few regions where neurogenesis persists in the adult brain is the SVZ of the lateral ventricules which provide new neurons to the olfactory bulb during adulthood. Cells from the SVZ proliferate and migrate via the rostral migratory stream to the olfactory bulb where they differentiate into neurons, mostly into granule cells, which integrate into the functional circuitry of the bulb (Lledo et al., 2008). Of relevance for taurine implication in neurogenesis, the olfactory bulb contains the highest taurine levels in the adult brain, and in contrast to most brain regions, there is no taurine decline during brain maturation (Miranda-Contreras et al., 2000). The high levels of taurine in the olfactory bulb may then respond to a requirement for the optimal proliferation, migration and differentiation of the NPCs in the adult brain.
    Materials and methods
    Acknowledgments We acknowledge the valuable technical assistance of Patricia Salazar Sandoval for HPLC measurements. We are grateful to Drs. Luis Covarrubias and Ivan Velasco for their most helpful comments and suggestions throughout this study. This work was supported by the Dirección General de Asuntos del Personal Académico (DGAPA), Universidad Nacional Autónoma de México (UNAM) [grant number IN203410], and Consejo Nacional de Ciencia y Tecnología (CONACyT) [grant number 98952]. This work is part of the requirements for the Ph.D. degree in Biomedical Sciences of Reyna Hernández-Benítez at UNAM, with a CONACyT fellowship.
    Introduction White adipose tissues are the primary triglyceride/energy storages of the body acting as metabolic regulator in glucose homeostasis and lipid metabolism (Rosen and Spiegelman, 2006), and as endocrine organ (Hauner, 2005). The main cell type in fat tissues fulfilling these functions is the mature adipocyte. In adult humans approximately 10% of fat cells in adipose depots are renewed annually (Spalding et al., 2008), and surgical removal of fat tissue in rodents induces compensatory recovery (Mauer et al., 2001). This indicates a high demand of progenitor cells for renewal and, hence, maintenance of adipose tissue functions. In fact, the number of adipocyte progenitors in a given fat tissue can vary between 15 and 40% of the cell population dependent on the tissue type, localization in the body, physiological conditions, and age (Bouloumie et al., 2008; Cartwright et al., 2010; Hauner, 2005).