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dc.creatorLeiguez, Elbio
dc.creatordo Nascimento Viana, Mariana
dc.creatorHideki Matsubara, Márcio
dc.creatorFernandes, Cristina Maria
dc.creatorGiannotti, Karina Cristina
dc.creatorGutiérrez, José María
dc.creatorLomonte, Bruno
dc.creatorTeixeira, Catarina de Fátima
dc.date.accessioned2019-02-01T21:13:30Z
dc.date.available2019-02-01T21:13:30Z
dc.date.issued2018-06
dc.identifier.citationhttps://www.hindawi.com/journals/mi/2018/2547918/es_ES
dc.identifier.issn0962-9351
dc.identifier.issn1466-1861
dc.identifier.urihttp://hdl.handle.net/10669/76538
dc.description.abstractMT-III, a snake venom GIIA sPLA2, which shares structural and functional features with mammalian GIIA sPLA2s, activates macrophage defense functions including lipid droplet (LDs) formation, organelle involved in both lipid metabolism and inflammatory processes. Macrophages (MΦs) loaded with LDs, termed foam cells, characterize early blood vessel fatty-streak lesions during atherosclerosis. However, the factors involved in foam cell formation induced by a GIIA sPLA2 are still unknown. Here, we investigated the participation of lipid homeostasis-related factors in LD formation induced by MT-III in macrophages. We found that MT-III activated PPAR-γ and PPAR-β/δ and increased the protein levels of both transcription factors and CD36 in macrophages. Pharmacological interventions evidenced that PPAR-γ, PPAR-β/δ, and CD36 as well as the endoplasmic reticulum enzymes ACAT and DGAT are essential for LD formation. Moreover, PPAR-β/δ, but not PPAR-γ, is involved in MT-III-induced PLIN2 protein expression, and both PPAR-β/δ and PPAR-γ upregulated CD36 protein expression, which contributes to MT-III-induced COX-2 expression. Furthermore, production of 15-d-PGJ2, an activator of PPARs, induced by MT-III, was dependent on COX-1 being LDs an important platform for generation of this mediator.es_ES
dc.description.sponsorshipFundación de Apoyo a la Investigación del Estado de São Paulo/[00 / 11624-5]/FAPESP/Brasiles_ES
dc.description.sponsorshipFundación de Apoyo a la Investigación del Estado de São Paulo/[2011 / 21341-5]/FAPESP/Brasiles_ES
dc.description.sponsorshipFundación de Apoyo a la Investigación del Estado de São Paulo/[2014 / 18549-1]/FAPESP/Brasiles_ES
dc.description.sponsorshipFundación de Apoyo a la Investigación del Estado de São Paulo/[2010 / 06345-1]/FAPESP/Brasiles_ES
dc.description.sponsorshipFundación de Apoyo a la Investigación del Estado de São Paulo/[2015 / 24701-3]/FAPESP/Brasiles_ES
dc.description.sponsorshipFundación de Apoyo a la Investigación del Estado de São Paulo/[2013 / 22610-5]/FAPESP/Brasiles_ES
dc.description.sponsorshipFundación de Apoyo a la Investigación del Estado de São Paulo/[2010 / 08506-2]/FAPESP/Brasiles_ES
dc.description.sponsorshipFundación de Apoyo a la Investigación del Estado de São Paulo/[307379 / 2016-7]/FAPESP/Brasiles_ES
dc.language.isoen_USes_ES
dc.sourceMediators of Inflammation, vol. 2018 ,pp. 1-13es_ES
dc.subjectSnakees_ES
dc.subjectVenomes_ES
dc.subjectPhospholipase A2es_ES
dc.subject615.946 Venenos animaleses_ES
dc.subjectVeneno de serpientees_ES
dc.titleA snake venom secreted phospholipase A2 induces foam cell formation depending on the activation of factors involved in lipid homeostasises_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.identifier.doi10.1155/2018/2547918
dc.description.procedenceUCR::Vicerrectoría de Investigación::Unidades de Investigación::Ciencias de la Salud::Instituto Clodomiro Picado (ICP)es_ES


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