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Macrophage migration inhibitory factor deficiency protects pancreatic islets from cytokine-induced apoptosis in vitro
dc.creator | Stojanović, Ivana D. | |
dc.creator | Saksida, Tamara | |
dc.creator | Nikolić, Ivana | |
dc.creator | Nicoletti, Ferdinando | |
dc.creator | Stošić-Grujičić, Stanislava | |
dc.date.accessioned | 2017-11-23T11:12:26Z | |
dc.date.available | 2015-11-17T10:26:51Z | |
dc.date.issued | 2012 | sr |
dc.identifier.issn | 0009-9104 | sr |
dc.identifier.other | Rad_konverzija_3150 | sr |
dc.identifier.uri | https://radar.ibiss.bg.ac.rs/handle/123456789/1155 | |
dc.description.abstract | During pathogenesis of diabetes, pancreatic islets are exposed to high levels of cytokines and other inflammatory mediators that induce deterioration of insulin-producing beta cells. Macrophage migration inhibitory factor (MIF) plays a key role in the onset and development of several immunoinflammatory diseases and also controls apoptotic cell death. Because the occurrence of apoptosis plays a pathogenetic role in beta cell death during type 1 diabetes development and MIF is expressed in beta cells, we explored the influence of MIF deficiency on cytokine-induced apoptosis in pancreatic islets. The results indicated clearly that elevated MIF secretion preceded C57BL/6 pancreatic islets death induced by interferon (IFN)-? + tumour necrosis factor (TNF)-a + interleukin (IL)-1 beta. Consequently, MIF-deficient [MIF-knock-out (KO)] pancreatic islets or islet cells showed significant resistance to cytokine-induced death than those isolated from C57BL/6 mice. Furthermore, upon exposure to cytokines pancreatic islets from MIF-KO mice maintained normal insulin expression and produced less cyclooxygenase-2 (COX-2) than those from wild-type C57BL6 mice. The final outcome of cytokine-induced islet apoptosis in islets from wild-type mice was the activation of mitochondrial membrane pore-forming protein Bcl-2-associated X protein and effector caspase 3. In contrast, these apoptotic mediators remained at normal levels in islets from MIF-KO mice suggesting that MIF absence prevented initiation of the mitochondrial apoptotic pathway. Additionally, the protection from apoptosis was also mediated by up-regulation of prosurvival kinase extracellular-regulated kinase 1/2 in MIF-KO islets. These data indicate that MIF is involved in the propagation of pancreatic islets apoptosis probably via nuclear factor-?B and mitochondria-related proteins. | en |
dc.description.sponsorship | Ministry of Education and Science, Republic of Serbia [173013] | sr |
dc.language.iso | English | sr |
dc.rights | restrictedAccess | |
dc.source | Clinical and Experimental Immunology | sr |
dc.title | Macrophage migration inhibitory factor deficiency protects pancreatic islets from cytokine-induced apoptosis in vitro | en |
dc.type | article | |
dc.rights.license | ARR | |
dcterms.abstract | Николић, Ивана; Ницолетти, Фердинандо; Стошић-Грујичић, Станислава Д.; Саксида, Тамара; Стојановић, Ивана Т; | |
dc.citation.issue | 2 | sr |
dc.citation.volume | 169 | sr |
dc.citation.spage | 365 | sr |
dc.citation.epage | 163 | sr |
dc.type.version | publishedVersion | en |
dc.citation.rank | M22 | |
dc.identifier.rcub | https://hdl.handle.net/21.15107/rcub_ibiss_1155 |
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