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dc.contributor.authorGómez Bahamonde, Rodolfo
dc.contributor.authorConde Aranda, Javier
dc.contributor.authorScotece, Morena
dc.contributor.authorLópez López, Verónica
dc.contributor.authorLago Paz, Francisca 
dc.contributor.authorGómez-Reino Carnota, Juan Jesús 
dc.contributor.authorGualillo ., Oreste 
dc.date.accessioned2017-06-07T07:16:38Z
dc.date.available2017-06-07T07:16:38Z
dc.date.issued2014
dc.identifier.issn0736-0266
dc.identifier.urihttp://hdl.handle.net/20.500.11940/4629
dc.description.abstractEndocannabinoids has been described to be involved in articular degenerative disease by modulating nociception and immune system. However, the role of the endocannabinoid anandamide on chondrocyte cell viability is still unclear. Therefore, we decided to study anandamide's effects on chondrocytes viability and to evaluate its interactions with the catabolic factor TNF (tumor necrosis factor). Chondrocyte vitality was evaluated by MTT assay. We investigated LDH release, chromatin condensation, cleavage of focal adhesion kinase (FAK), and caspases-3, 8, and 9 activation. c-MYC mRNA levels were determined by RT-PCR. We studied by Western blot the activation patterns of AKT, AMPK, ERK, p38, and JNK kinases. Finally, we evaluate the effect of anandamide in TNF-induced caspase-3 cleavage. Anandamide decreased chondrocyte vitality independently of its receptors. It induced AMPK activation without LDH release. Anandamide induced chromatin condensation, activation of caspase-3, 8, and 9, and FAK cleavage. Surprisingly, despite anandamide inhibited cell proliferation, it increased c-MYC expression. Moreover anandamide inhibited AKT activation, whilst it induced a sustained activation of ERK, JNK, and p38. Finally, anandamide synergized with TNF-alpha in the cleavage of caspase-3. In conclusion, our findings suggest that anandamide, alone or in combination with TNF-alpha, may be a potential destructive agent in cartilage.
dc.description.sponsorshipInstituto de Salud Carlos III
dc.description.sponsorshipXunta de Galicia (SERGAS)
dc.description.sponsorshipRETICS Programme, RD08/0075 (RIER) via Instituto de Salud Carlos III (ISCIII)
dc.description.sponsorship“FPU” programme of the Spanish Ministry of Education
dc.description.sponsorshipInstituto de Salud Carlos III (ISCIII)/ “Sara Borrell Programme”
dc.language.isoeng
dc.subject.meshAMP-Activated Protein Kinases
dc.subject.meshAnimals
dc.subject.meshApoptosis
dc.subject.meshArachidonic Acids
dc.subject.meshCannabinoids
dc.subject.meshCaspases
dc.subject.meshCell Line
dc.subject.meshCell Proliferation
dc.subject.meshChondrocytes
dc.subject.meshChromatin/drug effects
dc.subject.meshEndocannabinoids
dc.subject.meshMAP Kinase Signaling System
dc.subject.meshMice
dc.subject.meshModels, Animal
dc.subject.meshPolyunsaturated Alkamides
dc.subject.meshProto-Oncogene Proteins c-akt
dc.subject.meshSignal Transduction/drug effects
dc.subject.meshTumor Necrosis Factor-alpha
dc.subject.meshTnf|
dc.titleEndogenous cannabinoid anandamide impairs cell growth and induces apoptosis in chondrocytes
dc.typeArtigoes
dc.authorsophosGómez, R.
dc.authorsophosConde, J.
dc.authorsophosScotece, M.
dc.authorsophosLópez, V.
dc.authorsophosLago, F.
dc.authorsophosGómez Reino, J. J.
dc.authorsophosGualillo, O.
dc.identifier.doi10.1002/jor.22660
dc.identifier.isi340587200008
dc.identifier.pmid24902823
dc.identifier.sophos14697
dc.issue.number9
dc.journal.titleJOURNAL OF ORTHOPAEDIC RESEARCH
dc.organizationServizo Galego de Saúde::Estrutura de Xestión Integrada (EOXI)::EOXI de Santiago - Complexo Hospitalario Universitario de Santiago::Reumatoloxía
dc.organizationServizo Galego de Saúde::Estrutura de Xestión Integrada (EOXI)::EOXI de Santiago::IDIS.- Instituto de investigaciones sanitarias de Santiago
dc.page.initial1137
dc.page.final46
dc.relation.projectIDInstituto de Salud Carlos III/PI11/01073
dc.relation.projectIDXunta de Galicia/10CSA918029PR
dc.relation.projectIDInstituto de Salud Carlos III/PI11/00497
dc.relation.projectIDREDINSCOR/RD06/0003/0016
dc.rights.accessRightsopenAccess
dc.typesophosArtículo Original
dc.volume.number32


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