Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/70925
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dc.contributor.authorRajanbabu, V.en_US
dc.contributor.authorChen, J.Y.en_US
dc.date2011zh_TW
dc.date.accessioned2014-06-11T06:00:34Z-
dc.date.available2014-06-11T06:00:34Z-
dc.identifier.issn0196-9781zh_TW
dc.identifier.urihttp://hdl.handle.net/11455/70925-
dc.description.abstractThe antimicrobial and immunomodulatory functions of the antimicrobial peptide, tilapia hepcidin (TH)2-3, were previously studied. Herein, we report the differential modulation of protein kinase C (PKC)-associated proteins by TH2-3, and the PKC activator, phorbol 12-myristate 13-acetate (PMA), in RAW264.7 macrophages. Treatment with TH2-3 at 40 or 80 mu g/ml did not affect the cell morphology, but TH2-3 at 120 mu g/ml produced morphological changes similar to those after treatment with PMA in RAW264.7 cells. The coexistence of the PKC inhibitor, Ro-31-8220, prevented morphological changes induced by either PMA or 120 mu g/ml TH2-3 in RAW264.7 cells. Since PMA is known to induce expression of the proinflammatory cytokine, tumor necrosis factor (TNF)-alpha, activation of the TNF-alpha promoter in response to TH2-3 and PMA treatments in lipopolysaccharide (LPS)-stimulated cells was compared. In LPS-stimulated RAW264.7 cells, TNF-alpha promoter activity was significantly suppressed by TH2-3, but not by PMA. In addition, PMA activated prostaglandin synthase-associated cyclooxygenase (COX)-2 proteins on the cell surface, while the presence of TH2-3 inhibited its expression. Western blotting demonstrated that the expressions of PKC-mu, phosphorylated (p)-PKC mu at serine (S)-744, and p-PKC delta were activated by PMA, but were suppressed by TH2-3. In addition, p-PKC at S-916 was activated by TH2-3 and inhibited by PMA. In conclusion, the differential regulation of PKC isoforms by PMA and TH2-3 may influence morphological changes and regulation of TNF-alpha in RAW264.7 cells. (C) 2010 Elsevier Inc. All rights reserved.en_US
dc.language.isoen_USzh_TW
dc.relationPeptidesen_US
dc.relation.ispartofseriesPeptides, Volume 32, Issue 2, Page(s) 333-341.en_US
dc.relation.urihttp://dx.doi.org/10.1016/j.peptides.2010.11.004en_US
dc.subjectAntimicrobial peptideen_US
dc.subjectTilapia hepcidin 2-3en_US
dc.subjectPMAen_US
dc.subjectPKCen_US
dc.subjectTNF-alphaen_US
dc.subjectCOX-2en_US
dc.subjectdendritic-like cellsen_US
dc.subjectlipopolysaccharide-induced differentiationen_US
dc.subjectactivationen_US
dc.subjectphenotypeen_US
dc.subjectbindingen_US
dc.subjectsepsisen_US
dc.subjectlineen_US
dc.subjectlpsen_US
dc.titleThe antimicrobial peptide, tilapia hepcidin 2-3, and PMA differentially regulate the protein kinase C isoforms, TNF-alpha and COX-2, in mouse RAW264.7 macrophagesen_US
dc.typeJournal Articlezh_TW
dc.identifier.doi10.1016/j.peptides.2010.11.004zh_TW
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