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首页> 外文期刊>Journal of Cellular Physiology >The PPAR beta/delta Agonist GW0742 Induces Early Neuronal Maturation of Cortical Post-Mitotic Neurons: Role of PPAR beta/delta in Neuronal Maturation
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The PPAR beta/delta Agonist GW0742 Induces Early Neuronal Maturation of Cortical Post-Mitotic Neurons: Role of PPAR beta/delta in Neuronal Maturation

机译:PPARβ/δ受体激动剂GW0742诱发早神经皮质Post-Mitotic的成熟神经元:PPARβ/δ在神经元的作用成熟

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摘要

Increasing evidences support that signaling lipids participate in synaptic plasticity and cell survival, and that the lipid signaling is closely associated with neuronal differentiation, learning, and memory and with pathologic events, such as epilepsy and Alzheimer's disease. The Peroxisome Proliferator-Activated Receptors (PPAR) are strongly involved in the fatty acid cell signaling, as many of the natural lypophylic compounds are PPAR ligands. We have previously shown that PPAR/ is the main isotype present in cortical neuron primary cultures and that during neuronal maturation, PPAR/ is gradually increased and activated. To get more insight into the molecular mechanism by which PPAR/ may be involved in neuronal maturation processes, in this work a specific PPAR/ agonist, GW0742 was used administered alone or in association with a specific PPAR/ antagonist, the GSK0660, and the parameters involved in neuronal differentiation and maturation were assayed. The data obtained demonstrated the strong involvement of PPAR/ in neuronal maturation, triggering the agonist an anticipation of neuronal differentiation, and the antagonist abolishing the observed effects. These effects appear to be mediated by the activation of BDNF pathway. J. Cell. Physiol. 231: 597-606, 2016. (c) 2015 Wiley Periodicals, Inc.
机译:越来越多的证据支持脂质信号参与突触可塑性和细胞生存,脂质信号密切与神经元分化有关,学习、记忆和与病理事件,如癫痫、阿尔茨海默氏症。过氧物酶体Proliferator-Activated受体(PPAR)强烈参与脂肪酸细胞信号,尽可能多的自然lypophylic化合物是PPAR配体。表明,PPAR /主要同形像出现在皮质神经元主要文化和期间神经元的成熟,PPAR /正逐渐增加和激活。PPAR /可能的分子机制参与神经细胞成熟过程,这个工作具体PPAR激动剂,GW0742单独或与一个管理使用特定的PPAR /拮抗剂,GSK0660,参数参与神经元分化和成熟是化验。展示了强大的PPAR /参与神经元的成熟,引发的兴奋剂神经分化的期待,和拮抗剂废除观察效果。似乎是由激活的影响脑源性神经营养因子的途径。2016.

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