Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12104/45794
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dc.contributor.authorEttcheto M
dc.contributor.authorJunyent F
dc.contributor.authorde Lemos L
dc.contributor.authorPallas M
dc.contributor.authorFolch J
dc.contributor.authorBeas-Z�rate, Carlos
dc.contributor.authorVerdaguer E
dc.contributor.authorGomez-Sintes R
dc.contributor.authorLucas J.J
dc.contributor.authorAuladell C
dc.date.accessioned2015-09-15T19:20:14Z-
dc.date.available2015-09-15T19:20:14Z-
dc.date.issued2015
dc.identifier.urihttp://www.scopus.com/inward/record.url?eid=2-s2.0-84937850996&partnerID=40&md5=468079f94768e61b6deaf8d0fe421cc4
dc.identifier.urihttp://hdl.handle.net/20.500.12104/45794-
dc.description.abstractThe Fas receptor (FasR)/Fas ligand (FasL) system plays a significant role in the process of neuronal loss in neurological disorders. Thus, in the present study, we used a real-time PCR array focused apoptosis (Mouse Apoptosis RT2 PCR Array) to study the role of the Fas pathway in the apoptotic process that occurs in a kainic acid (KA) mice experimental model. In fact, significant changes in the transcriptional activity of a total of 23 genes were found in the hippocampus of wild-type C57BL/6 mice after 12�h of KA treatment compared to untreated mice. Among the up-regulated genes, we found key factors involved in the extrinsic apoptotic pathway, such as tnf, fas and fasL, and also in caspase genes (caspase-4, caspase-8 and caspase-3). To discern the importance of the FasR/FasL pathway, mice lacking the functional Fas death receptor (lpr) were also treated with KA. After 24�h of neurotoxin treatment, lpr mice exhibited a reduced number of apoptotic positive cells, determined by the terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) method in different regions of the hippocampus, when compared to wild-type mice. In addition, treatment of lpr mice with KA did not produce significant changes in the transcriptional activity of genes related to apoptosis in the hippocampus, either in the fas and fas ligand genes or in caspase-4 and caspase-8 and the executioner caspase-3 genes, as occurred in wild-type C57BL/6 mice. Thus, these data provide direct evidence that Fas signalling plays a key role in the induction of apoptosis in the hippocampus following KA treatment, making the inhibition of the death receptor pathway a potentially suitable target for excitotoxicity neuroprotection in neurological conditions such as epilepsy. � 2014, Springer Science+Business Media New York.
dc.relation.isreferencedbyScopus
dc.titleMice Lacking Functional Fas Death Receptors Are Protected from Kainic Acid-Induced Apoptosis in the Hippocampus
dc.typeArticle
dc.identifier.doi10.1007/s12035-014-8836-0
dc.relation.ispartofjournalMolecular Neurobiology
dc.relation.ispartofvolume52
dc.relation.ispartofissue1
dc.relation.ispartofpage120
dc.relation.ispartofpage129
dc.subject.keywordApoptosis; Caspase-3; FAS; Kainic acid; Microglia; Neuroprotection
dc.contributor.affiliationEttcheto, M., Unitat de Farmacologia i Farmacogn�sia Facultat de Farm�cia, Institut de Biomedicina (IBUB), Universitat de Barcelona, Avda/Diagonal 643, Barcelona, Spain, Networking Research Center on Neurodegenerative Diseases (CIBERNED), Instituto de Salud Carlos III, Madrid, Spain; Junyent, F., Unitat de Farmacologia i Farmacogn�sia Facultat de Farm�cia, Institut de Biomedicina (IBUB), Universitat de Barcelona, Avda/Diagonal 643, Barcelona, Spain, Networking Research Center on Neurodegenerative Diseases (CIBERNED), Instituto de Salud Carlos III, Madrid, Spain; de Lemos, L., Unitat de Farmacologia i Farmacogn�sia Facultat de Farm�cia, Institut de Biomedicina (IBUB), Universitat de Barcelona, Avda/Diagonal 643, Barcelona, Spain, Networking Research Center on Neurodegenerative Diseases (CIBERNED), Instituto de Salud Carlos III, Madrid, Spain; Pallas, M., Unitat de Farmacologia i Farmacogn�sia Facultat de Farm�cia, Institut de Biomedicina (IBUB), Universitat de Barcelona, Avda/Diagonal 643, Barcelona, Spain, Networking Research Center on Neurodegenerative Diseases (CIBERNED), Instituto de Salud Carlos III, Madrid, Spain; Folch, J., Networking Research Center on Neurodegenerative Diseases (CIBERNED), Instituto de Salud Carlos III, Madrid, Spain, Unitat de Bioqu�mica, Facultat de Medicina i Ci�ncies de la Salut, Universitat Rovira i Virgili, Reus, Tarragona, Spain; Beas-Zarate, C., Laboratorio de Neurobiolog�a Celular y Molecular, Divisi�n de Neurociencias, CIBO, IMSS, Guadalajara, Mexico, Laboratorio de Desarrollo y Regeneraci�n Neural, Instituto de Neurobiolog�a, Departamento de Biolog�a Celular y Molecular, CUCBA, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico; Verdaguer, E., Departament de Biologia Cel�lular, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain; G�mez-Sintes, R., Networking Research Center on Neurodegenerative Diseases (CIBERNED), Instituto de Salud Carlos III, Madrid, Spain, Center for Molecular Biology �Severo Ochoa� (CBMSO) CSIC/UAM, Madrid, Spain; Lucas, J.J., Networking Research Center on Neurodegenerative Diseases (CIBERNED), Instituto de Salud Carlos III, Madrid, Spain, Center for Molecular Biology �Severo Ochoa� (CBMSO) CSIC/UAM, Madrid, Spain; Auladell, C., Networking Research Center on Neurodegenerative Diseases (CIBERNED), Instituto de Salud Carlos III, Madrid, Spain, Departament de Biologia Cel�lular, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain; Camins, A., Unitat de Farmacologia i Farmacogn�sia Facultat de Farm�cia, Institut de Biomedicina (IBUB), Universitat de Barcelona, Avda/Diagonal 643, Barcelona, Spain, Networking Research Center on Neurodegenerative Diseases (CIBERNED), Instituto de Salud Carlos III, Madrid, Spain
dc.contributor.affiliationBeas-Z�rate, Carlos., Universidad de Guadalajara. Centro Universitario de Ciencias Biol�gicas y Agropecuarias
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