| Galectin-3 deficiency protects pancreatic islet cells from cytokine-triggered apoptosis in vitro. | |
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MedLine Citation:
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PMID: 23280610 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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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, 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. J. Cell. Physiol. © 2012 Wiley Periodicals, Inc. |
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Authors:
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Tamara Saksida; Ivana Nikolic; Milica Vujicic; Ulf J Nilsson; Hakon Leffler; Miodrag L Lukic; Ivana Stojanovic; Stanislava Stosic-Grujicic |
Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-12-31 |
Journal Detail:
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Title: Journal of cellular physiology Volume: - ISSN: 1097-4652 ISO Abbreviation: J. Cell. Physiol. Publication Date: 2012 Dec |
Date Detail:
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Created Date: 2013-1-2 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0050222 Medline TA: J Cell Physiol Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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Copyright © 2012 Wiley Periodicals, Inc. |
Affiliation:
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Department of Immunology, Institute for Biological Research "Siniša Stanković", University of Belgrade, Belgrade, Serbia. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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