Activation of NPFF2 receptor stimulates neurite outgrowth in Neuro 2A cells through activation of ERK signaling pathway |
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| Affiliation: | 1. Departamento de Toxicología y Farmacología, Facultad de Veterinaria, Universidad Complutense de Madrid, 28040 Madrid, Spain;2. Departamento de Bioquímica y Biología Molecular IV, Facultad de Veterinaria, Universidad Complutense de Madrid, 28040 Madrid, Spain;3. Instituto Universitario de Investigación en Neuroquímica, Universidad Complutense de Madrid, 28040 Madrid, Spain;4. Departamento de Medicina Preventiva, Salud Pública e Inmunología Médica y Microbiología. Facultad de Ciencias de la Salud, Universidad Rey Juan Carlos, 28922 Madrid, Spain;1. Discipline of Medicine, The University of Adelaide, South Australia, 5000, Australia;2. NHMRC Centre of Research Excellence in Translating Nutritional Science to Good Health, The University of Adelaide, South Australia, 5000, Australia;1. State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400716, China;2. Vitamin D Research Institute, Shaanxi Sci-Tech University, Hanzhong 723001, Shaanxi Province, China;3. College of Education Science, Shaanxi Sci-Tech University, Hanzhong 723001, Shaanxi Province, China;1. Laboratory of Neuroanatomy and Experimental Neurology, Dept. of Morphological Sciences, CIMUS, University of Santiago de Compostela, Santiago de Compostela, Spain;2. Networking Research Center on Neurodegenerative Diseases (CIBERNED), Spain |
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| Abstract: | Neurite outgrowth is an important process in neural regeneration and plasticity, especially after neural injury, and recent evidence indicates that several Gαi/o protein-coupled receptors play an important role in neurite outgrowth. The neuropeptide (NP)FF system contains two Gαi/o protein-coupled receptors, NPFF1 and NPFF2 receptors, which are mainly distributed in the central nervous system. The aim of the present study was to determine whether the NPFF system is involved in neurite outgrowth in Neuro 2A cells. We showed that Neuro 2A cells endogenously expressed NPFF2 receptor, and the NPFF2 receptor agonist dNPA inhibited cyclic adenosine monophosphate (cAMP) production stimulated by forskolin in Neuro 2A cells. We also demonstrated that NPFF and dNPA dose-dependently induced neurite outgrowth in Neuro 2A cells, which was completely abolished by the NPFF receptor antagonist RF9. Pretreatment with mitogen-activated protein kinase inhibitors PD98059 and U0126 decreased dNPA-induced neurite outgrowth. In addition, dNPA increased phosphorylation of extracellular signal-regulated kinase (ERK) in Neuro 2A cells, which was completely antagonized by pretreatment with U0126. Our results suggest that activation of NPFF2 receptor stimulates neurite outgrowth in Neuro 2A cells through activation of the ERK signaling pathway. Moreover, NPFF2 receptor may be a potential therapeutic target for neural injury and degeneration in the future. |
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| Keywords: | Neurite outgrowth Neuro 2A cells MEK/ERK signaling pathway |
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