Please use this identifier to cite or link to this item: https://scidar.kg.ac.rs/handle/123456789/10281
Title: Galectin-3 deficiency protects pancreatic islet cells from cytokine-triggered apoptosis in vitro
Authors: Saksida, Tamara
Nikolić, Ivana
Vujičić, Milica
Nilsson U.
Leffler, Hakon
Lukic, Miodrag
Stojanović, Ivana
Stosic-Grujicic, Stanislava
Journal: Journal of Cellular Physiology
Issue Date: 1-Jul-2013
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, β-lactose or TD139, supported survival and function of islet beta cells compromised by TNF-α+IFN-γ+IL-1β stimulus. Similarly, inhibition of galectin-3 by β-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. © 2012 Wiley Periodicals, Inc.
URI: https://scidar.kg.ac.rs/handle/123456789/10281
Type: article
DOI: 10.1002/jcp.24318
ISSN: 00219541
SCOPUS: 84875509705
Appears in Collections:Faculty of Medical Sciences, Kragujevac

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