Logotipo del repositorio
  • English
  • Español
  • Iniciar sesión
    ¿Nuevo Usuario? Pulse aquí para registrarse¿Has olvidado tu contraseña?
Logotipo del repositorio
  • English
  • Español
  • Iniciar sesión
    ¿Nuevo Usuario? Pulse aquí para registrarse¿Has olvidado tu contraseña?
  1. Inicio
  2. Buscar por autor

Examinando por Autor "Garcia-Segura, L.M."

Mostrando 1 - 4 de 4
Resultados por página
Opciones de ordenación
  • Cargando...
    Miniatura
    ÍtemAcceso Abierto
    Neuroprotective effects of the catalytic subunit of telomerase: a potential therapeutic target in the central nervous system
    (Elsevier Ireland Ltd, 2016) González-Giraldo, Y.; Forero, D.A.; Echeverria, V.; Gonzalez, J.; Ávila-Rodriguez, M.; Garcia-Segura, L.M.; Barreto, G.E.
    Senescence plays an important role in neurodegenerative diseases and involves key molecular changes induced by several mechanisms such as oxidative stress, telomere shortening and DNA damage. Potential therapeutic strategies directed to counteract these molecular changes are of great interest for the prevention of the neurodegenerative process. Telomerase is a ribonucleoprotein composed of a catalytic subunit (TERT) and a RNA subunit (TERC). It is known that the telomerase is involved in the maintenance of telomere length and is a highly expressed protein in embryonic stages and decreases in adult cells. In the last decade, a growing number of studies have shown that TERT has neuroprotective effects in cellular and animal models after a brain injury. Significantly, differences in TERT expression between controls and patients with major depressive disorder have been observed. More recently, TERT has been associated with the decrease in reactive oxygen species and DNA protection in mitochondria of neurons. In this review, we highlight the role of TERT in some neurodegenerative disorders and discuss some studies focusing on this protein as a potential target for neuroprotective therapies. © 2016 Elsevier B.V.
  • Cargando...
    Miniatura
    ÍtemAcceso Abierto
    Regulation of astroglia by gonadal steroid hormones under physiological and pathological conditions
    (2016) Acaz-Fonseca E.; Avila-Rodriguez, M.; Garcia-Segura, L.M.; Barreto, G.E.
    In the last years there has been a considerable advance in the knowledge on the regulation of astrocytes by sex steroids under physiological and pathological conditions. By the activation of a variety of nuclear and membrane receptors, sex steroid hormones regulate the functions of astrocytes and their communication with other cell types in the central nervous system. Under physiological conditions astrocytes participate in the neuroendocrine and behavioral actions of gonadal steroids, as well as in the hormonal control of brain tissue homeostasis. Under pathological conditions astrocytes mediate, at least partially, the neuroprotective effects of gonadal steroid hormones; given that sex steroids modulate reactive astrogliosis and reduce the release of pro-inflammatory molecules by these cells. Given the side effects that sex steroids may have when administered systemically, a number of synthetic agonists of the receptors for gonadal steroid hormones in the nervous system have been developed, and may be considered for clinical use after brain injury as potential enhancers of the neuroprotective astrocytic functions. © 2016 Elsevier Ltd
  • Cargando...
    Miniatura
    ÍtemAcceso Abierto
    Testosterone protects mitochondrial function and regulates neuroglobin expression in astrocytic cells exposed to glucose deprivation
    (Frontiers Research Foundation, 2016) Toro-Urrego, N.; Garcia-Segura, L.M.; Echeverria, V.; Barreto, G.E.
    Testosterone is a hormone that has been shown to confer neuroprotection from different insults affecting the central nervous system (CNS). Testosterone induces this protection by different mechanisms that include the activation of anti-apoptotic pathways that are directly implicated in neuronal survival. However, little attention has been devoted to its actions on glial cells. In the present study, we have assessed whether testosterone exerts protection in a human astrocyte cell model, the T98G cells. Our results indicate that testosterone improves cell survival and mitochondrial membrane potential and reduces nuclear fragmentation and reactive oxygen species (ROS) generation. These effects were accompanied by a positive regulation of neuroglobin, an oxygen-binding and sensor protein, which may serve as a regulator of ROS and nitrogen reactive species (NOS), and these protective effects of testosterone may be at least in part mediated by estradiol and DHT. In conclusion, these findings suggest that astroglia may mediate some of the protective actions of testosterone in the brain upon pathological conditions. © 2016 Toro-Urrego, Garcia-Segura, Echeverria and Barreto.
  • Cargando...
    Miniatura
    ÍtemAcceso Abierto
    Tibolone protects astrocytic cells from glucose deprivation through a mechanism involving estrogen receptor beta and the upregulation of neuroglobin expression
    (Elsevier Ireland Ltd, 2016) Avila-Rodriguez, M.; Garcia-Segura, L.M.; Hidalgo-lanussa, O.; Baez, E.; Gonzalez, J.; Barreto, G.E.
    Tibolone, a synthetic steroid used for the prevention of osteoporosis and the treatment of climacteric symptoms in post-menopausal women, may exert tissue selective estrogenic actions acting on estrogen receptors (ERs). We previously showed that tibolone protects human T98G astroglial cells against glucose deprivation (GD). In this study we have explored whether the protective effect of tibolone on these cells is mediated by ERs. Experimental studies showed that both ERα and ERβ were involved in the protection by tibolone on GD cells, being ERβ preferentially involved on these actions over ERα. Tibolone increased viability of GD cells by a mechanism fully blocked by an ERβ antagonist and partially blocked by an ERα antagonist. Furthermore, ERβ inhibition prevented the effect of tibolone on nuclear fragmentation, ROS and mitochondrial membrane potential in GD cells. The protective effect of tibolone was mediated by neuroglobin. Tibolone upregulated neuroglobin in T98G cells and primary mouse astrocytes by a mechanism involving ERβ and neuroglobin silencing prevented the protective action of tibolone on GD cells. In summary, tibolone protects T98G cells by a mechanism involving ERβ and the upregulation of neuroglobin. © 2016 Elsevier Ireland Ltd.
Biblioteca Científica
Panamericana Sur Km. 19, Villa
  • 934792175
  • biblioteca@cientifica.edu.pe
DSpace, versión 7.6.1