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Galectin-3 deficiency protects pancreatic islet cells from cytokine-triggered apoptosis in vitro
dc.creator | Saksida, Tamara | |
dc.creator | Nikolić, Ivana | |
dc.creator | Vujičić, Milica | |
dc.creator | Nilsson, Ulf J | |
dc.creator | Leffler, Hakon | |
dc.creator | Lukić, Miodrag L | |
dc.creator | Stojanović, Ivana D. | |
dc.creator | Stošić-Grujičić, Stanislava | |
dc.date.accessioned | 2017-11-23T11:11:40Z | |
dc.date.available | 2015-11-17T10:26:51Z | |
dc.date.issued | 2013 | sr |
dc.identifier.issn | 0021-9541 | sr |
dc.identifier.other | Rad_konverzija_2990 | sr |
dc.identifier.uri | https://radar.ibiss.bg.ac.rs/handle/123456789/995 | |
dc.description.abstract | Beta cell apoptosis is a hallmark of diabetes. Since we have previously shown that galectin-3 deficient (LGALS3/) mice are relatively resistant to diabetes induction, the aim of this study was to examine whether beta cell apoptosis depends on the presence of galectin-3 and to delineate the underlying mechanism. Deficiency of galectin-3, either hereditary or induced through application of chemical inhibitors, -lactose or TD139, supported survival and function of islet beta cells compromised by TNF-+IFN-+IL-1 stimulus. Similarly, inhibition of galectin-3 by -lactose or TD139 reduced cytokine-triggered apoptosis of beta cells, leading to conclusion that endogenous galectin-3 propagates beta apoptosis in the presence of an inflammatory milieu. Exploring apoptosis-related molecules expression in primary islet cells before and after treatment with cytokines we found that galectin-3 ablation affected the expression of major components of mitochondrial apoptotic pathway, such as BAX, caspase-9, Apaf, SMAC, caspase-3, and AIF. In contrast, anti-apoptotic molecules Bcl-2 and Bcl-XL were up-regulated in LGALS3/ islet cells when compared to wild-type (WT) counterparts (C57BL/6), resulting in increased ratio of anti-apoptotic versus pro-apoptotic molecules. However, Fas-triggered apoptotic pathway as well as extracellular signal-regulated kinase 1/2 (ERK1/2) was not influenced by LGALS-3 deletion. All together, these results point to an important role of endogenous galectin-3 in beta cell apoptosis in the inflammatory milieu that occurs during diabetes pathogenesis and implicates impairment of mitochondrial apoptotic pathway as a key event in protection from beta cell apoptosis in the absence of galectin-3. J. Cell. Physiol. 228: 15681576, 2013. (c) 2012 Wiley Periodicals, Inc. | en |
dc.description.sponsorship | Ministry of Education and Science, Serbia [173013, 175069]; Serbian Ministry of Education, Science and Technological Development [173013, 175069] | sr |
dc.language.iso | English | sr |
dc.rights | restrictedAccess | |
dc.source | Journal of Cellular Physiology | sr |
dc.title | Galectin-3 deficiency protects pancreatic islet cells from cytokine-triggered apoptosis in vitro | en |
dc.type | article | |
dc.rights.license | ARR | |
dcterms.abstract | Стојановић, Ивана Т; Лукић, Миодраг Л; Николић, Ивана; Саксида, Тамара; Вујичић, Милица; Стошић-Грујичић, Станислава Д.; Нилссон, Улф Ј; Леффлер, Хакон; | |
dc.citation.issue | 7 | sr |
dc.citation.volume | 228 | sr |
dc.citation.spage | 25 | sr |
dc.citation.epage | 1576 | sr |
dc.type.version | publishedVersion | en |
dc.citation.rank | M21 | |
dc.identifier.rcub | https://hdl.handle.net/21.15107/rcub_ibiss_995 |
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