Navegando por Palavras-chave "neurite outgrowth"

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    Cellular prion protein binds laminin and mediates neuritogenesis
    (Elsevier B.V., 2000-03-10) Graner, E.; Mercadante, A. F.; Zanata, S. M.; Forlenza, O. V.; Cabral, ALB; Veiga, S. S.; Juliano, M. A.; Roesler, R.; Walz, R.; Minetti, A.; Izquierdo, I; Martins, V. R.; Brentani, R. R.; Ludwig Inst Canc Res; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP); UFRGS; Ctr Tratamento; Pesquisa Hosp Canc
    Laminin (LN) plays a major role in neuronal differentiation, migration and survival. Here, we show that the cellular prion protein (PrPc) is a saturable, specific, high-affinity receptor for LN. the PrPc-LN interaction is involved in the neuritogenesis induced by NGF plus LN in the PC-12 cell line and the binding site resides in a carboxy-terminal decapeptide from the gamma-1 LN chain. Neuritogenesis induced by LN or its gamma-1-derived peptide in primary cultures from rat or either wild type or PrP null mice hippocampal neurons, indicated that PrPc is the main cellular receptor for that particular LN domain. These results point out to the importance of the PrPc-LN interaction for the neuronal plasticity mechanism. (C) 2000 Elsevier Science B.V. All rights reserved.
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    Thyroid hormone treated astrocytes induce maturation of cerebral cortical neurons through modulation of proteoglycan levels
    (Frontiers Research Foundation, 2013-08-12) Dezonne, Romulo S.; Stipursky, Joice; Araujo, Ana P. B.; Nones, Jader; Pavao, Mauro S. G.; Porcionatto, Marimelia [UNIFESP]; Gomes, Flavia C. A.; Universidade Federal do Rio de Janeiro (UFRJ); Universidade Federal de São Paulo (UNIFESP)
    Proper brain neuronal circuitry formation and synapse development is dependent on specific cues, either genetic or epigenetic, provided by the surrounding neural environment. Within the sesignals, thyroid hormones (T3 and T4) play crucial role in several steps of brain morphogenesis including proliferation of progenitor cells, neuronal differentiation, maturation, migration, and synapse formation. the lack of thyroid hormones during childhood is associated with several impair neuronal connections, cognitive deficits, and mental disorders. Many of the thyroid hormones effects are mediated by astrocytes, although the mechanisms underlying these events are still unknown. in this work, we investigated the effect of 3,5,3'-triiodothyronine-treated (T3-treated) astrocytes on cerebral cortex neuronal differentiation. Culture of neural progenitors from embryonic cerebral cortex mice onto T3-treated astrocyte monolayers yielded an increment in neuronal population, followed by enhancement of neuronal maturation, arborization and neurite outgrowth. in addition, real time PCR assays revealed an increase in the levels of the heparan sulfate proteoglycans, Glypican 1(GPC-1) and Syndecans 3 e 4 (SDC-3 e SDC-4), followed by a decrease in the levels of the chondroitin sulfate proteoglycan, Versican. Disruption of glycosaminoglycan chains by chondroitinase AC or heparanase III completely abolished the effects of T3-treated astrocytes on neuronal morphogenesis. Our work provides evidence that astrocytes are key mediators of T3 actions on cerebral cortex neuronal development and identified potential molecules and pathways involved in neurite extension; which might eventually contribute to a better understanding of axonal regeneration, synapse formation, and neuronal circuitry recover.