Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/85852
Type: Artigo de periódico
Title: An Asp49 Phospholipase A2 From Snake Venom Induces Cyclooxygenase-2 Expression And Prostaglandin E2 Production Via Activation Of Nf- κ B, P38mapk, And Pkc In Macrophages
Author: Moreira V.
Lomonte B.
Vinolo M.A.R.
Curi R.
Gutierrez J.M.
Teixeira C.
Abstract: Phospholipases A2 (PLA2) are key enzymes for production of lipid mediators. We previously demonstrated that a snake venom sPLA2 named MT-III leads to prostaglandin (PG)E2 biosynthesis in macrophages by inducing the expression of cyclooxygenase-2 (COX-2). Herein, we explored the molecular mechanisms and signaling pathways leading to these MT-III-induced effects. Results demonstrated that MT-III induced activation of the transcription factor NF-κB in isolated macrophages. By using NF-κB selective inhibitors, the involvement of this factor in MT-III-induced COX-2 expression and PGE2 production was demonstrated. Moreover, MT-III-induced COX-2 protein expression and PGE 2 release were attenuated by pretreatment of macrophages with SB202190, and Ly294002, and H-7-dihydro compounds, indicating the involvement of p38MAPK, PI3K, and PKC pathways, respectively. Consistent with this, MT-III triggered early phosphorylation of p38MAPK, PI3K, and PKC. Furthermore, SB202190, H-7-dihydro, but not Ly294002 treatment, abrogated activation of NF-κB induced by MT-III. Altogether, these results show for the first time that the induction of COX-2 protein expression and PGE2 release, which occur via NF-κB activation induced by the sPLA2-MT-III in macrophages, are modulated by p38MAPK and PKC, but not by PI3K signaling proteins. © 2014 Vanessa Moreira et al.
Editor: Hindawi Publishing Corporation
Rights: aberto
Identifier DOI: 10.1155/2014/105879
Address: http://www.scopus.com/inward/record.url?eid=2-s2.0-84899949347&partnerID=40&md5=73d83cc9bc0e19e0fcbadfe06baed313
Date Issue: 2014
Appears in Collections:Unicamp - Artigos e Outros Documentos

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