Galectin-3 deficiency protects pancreatic islet cells from cytokine-triggered apoptosis in vitro

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Saksida, Tamara (author)

Galectin-3 deficiency protects pancreatic islet cells from cytokine-triggered apoptosis in vitro

Article/chapterEnglish2013

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2013-03-21
Wiley,2013

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LIBRIS-ID:oai:lup.lub.lu.se:3bc193f8-8486-4b01-9e99-b35d1ae4cef1
https://lup.lub.lu.se/record/3749579URI
https://doi.org/10.1002/jcp.24318DOI

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Language:English
Summary in:English

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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.

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Nikolic, Ivana (author)
Vujicic, Milica (author)
Nilsson, UlfLund University,Lunds universitet,Centrum för analys och syntes,Kemiska institutionen,Institutioner vid LTH,Lunds Tekniska Högskola,Centre for Analysis and Synthesis,Department of Chemistry,Departments at LTH,Faculty of Engineering, LTH(Swepub:lu)ok2-uni (author)
Leffler, HakonLund University,Lunds universitet,Avdelningen för mikrobiologi, immunologi och glykobiologi - MIG,Institutionen för laboratoriemedicin,Medicinska fakulteten,Division of Microbiology, Immunology and Glycobiology - MIG,Department of Laboratory Medicine,Faculty of Medicine(Swepub:lu)mmb-hle (author)
Lukic, Miodrag L. (author)
Stojanovic, Ivana (author)
Stosic-Grujicic, Stanislava (author)
Centrum för analys och syntesKemiska institutionen (creator_code:org_t)

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In:Journal of Cellular Physiology: Wiley228:7, s. 1568-15761097-46520021-9541

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