TY  - JOUR
AU  - Saksida, Tamara
AU  - Nikolić, Ivana
AU  - Vujičić, Milica
AU  - Nilsson, Ulf J
AU  - Leffler, Hakon
AU  - Lukić, Miodrag L
AU  - Stojanović, Ivana D.
AU  - Stošić-Grujičić, Stanislava
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/995
AB  - 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.
T2  - Journal of Cellular Physiology
T1  - Galectin-3 deficiency protects pancreatic islet cells from cytokine-triggered apoptosis in vitro
IS  - 7
VL  - 228
SP  - 25
EP  - 1576
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_995
ER  - 

@article{
author = "Saksida, Tamara and Nikolić, Ivana and Vujičić, Milica and Nilsson, Ulf J and Leffler, Hakon and Lukić, Miodrag L and Stojanović, Ivana D. and Stošić-Grujičić, Stanislava",
year = "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, -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.",
journal = "Journal of Cellular Physiology",
title = "Galectin-3 deficiency protects pancreatic islet cells from cytokine-triggered apoptosis in vitro",
number = "7",
volume = "228",
pages = "25-1576",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_995"
}

Saksida, T., Nikolić, I., Vujičić, M., Nilsson, U. J., Leffler, H., Lukić, M. L., Stojanović, I. D.,& Stošić-Grujičić, S.. (2013). Galectin-3 deficiency protects pancreatic islet cells from cytokine-triggered apoptosis in vitro. in Journal of Cellular Physiology, 228(7), 25-1576.
https://hdl.handle.net/21.15107/rcub_ibiss_995

Saksida T, Nikolić I, Vujičić M, Nilsson UJ, Leffler H, Lukić ML, Stojanović ID, Stošić-Grujičić S. Galectin-3 deficiency protects pancreatic islet cells from cytokine-triggered apoptosis in vitro. in Journal of Cellular Physiology. 2013;228(7):25-1576.
https://hdl.handle.net/21.15107/rcub_ibiss_995 .

Saksida, Tamara, Nikolić, Ivana, Vujičić, Milica, Nilsson, Ulf J, Leffler, Hakon, Lukić, Miodrag L, Stojanović, Ivana D., Stošić-Grujičić, Stanislava, "Galectin-3 deficiency protects pancreatic islet cells from cytokine-triggered apoptosis in vitro" in Journal of Cellular Physiology, 228, no. 7 (2013):25-1576,
https://hdl.handle.net/21.15107/rcub_ibiss_995 .