TY  - CONF
AU  - Petrović, Ivica
AU  - Pejnović, Nada
AU  - Ljujić, Biljana
AU  - Pavlović, Slađana
AU  - Miletić Kovačević, Marina
AU  - Jeftić, IIlija
AU  - Đukić, Aleksandar
AU  - Selaković, Dragica
AU  - Draginić, Nevena
AU  - Anđić, Marijana
AU  - Jovičić, Nemanja
AU  - Lukić, Miodrag L.
PY  - 2021
UR  - https://onlinelibrary.wiley.com/toc/15214141/2021/51/S1
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/4878
AB  - During obesity hematopoetic cells‐derived galectin 3 induces insulin resistence. While the role of galectin 3 expressed in islet invading immune cells in both type of diabetes has been studied, the importance of expression of this molecule on the target pancreatic beta cells is not defined. We have used 10‐12 weeks old C57/BL6 male mice (WT) and C57/ BL6 mice with transgenically enhanced Gal‐3 expression in pancreatic β cells (TG). Obesity was induced with 16 weeks high fat diet regime. Pancreatic beta cells were tested for susceptibility to apoptosis induced by non‐esterified fatty acids and cytokines as well as parameters of oxidative stress. The overexpression of galectin 3 increases beta cells apoptosis in HFD conditions and increases the percentage of proinflammatory F4/80+ macrophages in islets that express galectin 3 and TLR4. In isolated islets, we have shown that galectin 3 overexpression increases cytokine and palmitate‐triggered beta cells apoptosis and also increases NO2‐ induced oxidative stress of beta cells. Also, in pancreatic lymph nodes, macrophages were shifted towards proinflammatory TNF‐α producing phenotype. By complementary approach in vivo and in vitro, we have shown that galectin 3 overexpression facilitates beta cell damage, enhances cytokine and palmitate‐triggered beta cells apoptosis and also increases NO2‐ induced oxidative stress in beta cells. Further, the results suggest that increased expression of galectin 3 in the pancreatic beta cells affects the metabolism of glucose and glycoregulation in mice on HFD, affecting the fasting glycemic values, as well as glycemia after glucose loading.
PB  - Wiley‐VCH GmbH
C3  - 6th European Congress of Immunology; 2021 Sep 1-4; Virtual Meeting
T1  - Overexpression of galectin 3 in pancreatic beta cells amplifies beta cell apoptosis and islet inflammation in type 2 diabetes in mice
DO  - 10.1002/eji.202170200
SP  - 366
ER  - 

@conference{
author = "Petrović, Ivica and Pejnović, Nada and Ljujić, Biljana and Pavlović, Slađana and Miletić Kovačević, Marina and Jeftić, IIlija and Đukić, Aleksandar and Selaković, Dragica and Draginić, Nevena and Anđić, Marijana and Jovičić, Nemanja and Lukić, Miodrag L.",
year = "2021",
abstract = "During obesity hematopoetic cells‐derived galectin 3 induces insulin resistence. While the role of galectin 3 expressed in islet invading immune cells in both type of diabetes has been studied, the importance of expression of this molecule on the target pancreatic beta cells is not defined. We have used 10‐12 weeks old C57/BL6 male mice (WT) and C57/ BL6 mice with transgenically enhanced Gal‐3 expression in pancreatic β cells (TG). Obesity was induced with 16 weeks high fat diet regime. Pancreatic beta cells were tested for susceptibility to apoptosis induced by non‐esterified fatty acids and cytokines as well as parameters of oxidative stress. The overexpression of galectin 3 increases beta cells apoptosis in HFD conditions and increases the percentage of proinflammatory F4/80+ macrophages in islets that express galectin 3 and TLR4. In isolated islets, we have shown that galectin 3 overexpression increases cytokine and palmitate‐triggered beta cells apoptosis and also increases NO2‐ induced oxidative stress of beta cells. Also, in pancreatic lymph nodes, macrophages were shifted towards proinflammatory TNF‐α producing phenotype. By complementary approach in vivo and in vitro, we have shown that galectin 3 overexpression facilitates beta cell damage, enhances cytokine and palmitate‐triggered beta cells apoptosis and also increases NO2‐ induced oxidative stress in beta cells. Further, the results suggest that increased expression of galectin 3 in the pancreatic beta cells affects the metabolism of glucose and glycoregulation in mice on HFD, affecting the fasting glycemic values, as well as glycemia after glucose loading.",
publisher = "Wiley‐VCH GmbH",
journal = "6th European Congress of Immunology; 2021 Sep 1-4; Virtual Meeting",
title = "Overexpression of galectin 3 in pancreatic beta cells amplifies beta cell apoptosis and islet inflammation in type 2 diabetes in mice",
doi = "10.1002/eji.202170200",
pages = "366"
}

Petrović, I., Pejnović, N., Ljujić, B., Pavlović, S., Miletić Kovačević, M., Jeftić, I., Đukić, A., Selaković, D., Draginić, N., Anđić, M., Jovičić, N.,& Lukić, M. L.. (2021). Overexpression of galectin 3 in pancreatic beta cells amplifies beta cell apoptosis and islet inflammation in type 2 diabetes in mice. in 6th European Congress of Immunology; 2021 Sep 1-4; Virtual Meeting
Wiley‐VCH GmbH., 366.
https://doi.org/10.1002/eji.202170200

Petrović I, Pejnović N, Ljujić B, Pavlović S, Miletić Kovačević M, Jeftić I, Đukić A, Selaković D, Draginić N, Anđić M, Jovičić N, Lukić ML. Overexpression of galectin 3 in pancreatic beta cells amplifies beta cell apoptosis and islet inflammation in type 2 diabetes in mice. in 6th European Congress of Immunology; 2021 Sep 1-4; Virtual Meeting. 2021;:366.
doi:10.1002/eji.202170200 .

Petrović, Ivica, Pejnović, Nada, Ljujić, Biljana, Pavlović, Slađana, Miletić Kovačević, Marina, Jeftić, IIlija, Đukić, Aleksandar, Selaković, Dragica, Draginić, Nevena, Anđić, Marijana, Jovičić, Nemanja, Lukić, Miodrag L., "Overexpression of galectin 3 in pancreatic beta cells amplifies beta cell apoptosis and islet inflammation in type 2 diabetes in mice" in 6th European Congress of Immunology; 2021 Sep 1-4; Virtual Meeting (2021):366,
https://doi.org/10.1002/eji.202170200 . .

TY  - CONF
AU  - Jovičić, Nemanja
AU  - Petrović, Ivica
AU  - Pejnović, Nada
AU  - Ljujić, Biljana
AU  - Miletić Kovačević, Marina
AU  - Pavlović, Slađana
AU  - Jeftić, Ilija
AU  - Đukić, Aleksandar
AU  - Srejović, Ivan
AU  - Selaković, Dragica
AU  - Jakovljević, Vladimir
AU  - Lukić, Miodrag L.
PY  - 2021
UR  - https://onlinelibrary.wiley.com/toc/15214141/2021/51/S1
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/4880
AB  - Galectin 3 (gal 3) has diverse roles in inflammatory and autoimmune diseases. There is evidence that galectin 3 plays a role in both, type 1 and type 2 diabetes. While the role of Gal‐3 expression in immune cells in experimental type 1 diabetes has been already studied, the importance of the overexpression of Gal‐3 in the target β cells is not defined. We used 10‐12 weeks old C57/BL6 male mice (WT) and C57/BL6 mice with transgenically enhanced Gal‐3 expression in pancreatic β cells (TG). Both groups, received STZ for 5 consecutive days at a dose of 40 mg/kg ip. Mice received exogenous mouse IL‐33 (0.4 μg/injection) i.p., 12th, 14 th, 16 th, and 18 th day after the disease induction. Control animals were treated with intraperitoneally PBS + citrate buffer or IL‐33 + citrate buffer. The overexpression of Gal‐3 protected β cells from apoptosis and attenuated MLD‐STZ induced hyperglycemia, glycosuria and ketonuria. The cellular analysis of pancreata and draining lymph nodes showed that Gal‐ 3 overexpression significantly decreased the number of proinflammatory cells without affecting T regulatory cells. The application of exogenous IL‐33, attenuates the development of disease, by increasing the presence of regulatory FoxP3+ ST2+ cells, and competely abrogate diabetogenesis. We demonstrated the potential synergistic effect of exogenous IL‐33 and TG overexpression of Gal‐3 in β cells Not only enhanced expresion of Gal‐3 in β cells reduced T cell mediated autoimmune inflammatory disease, but also exogenous IL‐33 application had powerful terapeutic effect in TG mice.
PB  - Wiley‐VCH GmbH
C3  - 6th European Congress of Immunology; 2021 Sep 1-4; Virtual Meeting
T1  - Transgenic Overexpression of Galectin-3 in Pancreatic β Cells Attenuates Hyperglycemia in Mice: Synergistic Antidiabetic Effect With Exogenous IL-33.
DO  - 10.1002/eji.202170200
SP  - 378
ER  - 

@conference{
author = "Jovičić, Nemanja and Petrović, Ivica and Pejnović, Nada and Ljujić, Biljana and Miletić Kovačević, Marina and Pavlović, Slađana and Jeftić, Ilija and Đukić, Aleksandar and Srejović, Ivan and Selaković, Dragica and Jakovljević, Vladimir and Lukić, Miodrag L.",
year = "2021",
abstract = "Galectin 3 (gal 3) has diverse roles in inflammatory and autoimmune diseases. There is evidence that galectin 3 plays a role in both, type 1 and type 2 diabetes. While the role of Gal‐3 expression in immune cells in experimental type 1 diabetes has been already studied, the importance of the overexpression of Gal‐3 in the target β cells is not defined. We used 10‐12 weeks old C57/BL6 male mice (WT) and C57/BL6 mice with transgenically enhanced Gal‐3 expression in pancreatic β cells (TG). Both groups, received STZ for 5 consecutive days at a dose of 40 mg/kg ip. Mice received exogenous mouse IL‐33 (0.4 μg/injection) i.p., 12th, 14 th, 16 th, and 18 th day after the disease induction. Control animals were treated with intraperitoneally PBS + citrate buffer or IL‐33 + citrate buffer. The overexpression of Gal‐3 protected β cells from apoptosis and attenuated MLD‐STZ induced hyperglycemia, glycosuria and ketonuria. The cellular analysis of pancreata and draining lymph nodes showed that Gal‐ 3 overexpression significantly decreased the number of proinflammatory cells without affecting T regulatory cells. The application of exogenous IL‐33, attenuates the development of disease, by increasing the presence of regulatory FoxP3+ ST2+ cells, and competely abrogate diabetogenesis. We demonstrated the potential synergistic effect of exogenous IL‐33 and TG overexpression of Gal‐3 in β cells Not only enhanced expresion of Gal‐3 in β cells reduced T cell mediated autoimmune inflammatory disease, but also exogenous IL‐33 application had powerful terapeutic effect in TG mice.",
publisher = "Wiley‐VCH GmbH",
journal = "6th European Congress of Immunology; 2021 Sep 1-4; Virtual Meeting",
title = "Transgenic Overexpression of Galectin-3 in Pancreatic β Cells Attenuates Hyperglycemia in Mice: Synergistic Antidiabetic Effect With Exogenous IL-33.",
doi = "10.1002/eji.202170200",
pages = "378"
}

Jovičić, N., Petrović, I., Pejnović, N., Ljujić, B., Miletić Kovačević, M., Pavlović, S., Jeftić, I., Đukić, A., Srejović, I., Selaković, D., Jakovljević, V.,& Lukić, M. L.. (2021). Transgenic Overexpression of Galectin-3 in Pancreatic β Cells Attenuates Hyperglycemia in Mice: Synergistic Antidiabetic Effect With Exogenous IL-33.. in 6th European Congress of Immunology; 2021 Sep 1-4; Virtual Meeting
Wiley‐VCH GmbH., 378.
https://doi.org/10.1002/eji.202170200

Jovičić N, Petrović I, Pejnović N, Ljujić B, Miletić Kovačević M, Pavlović S, Jeftić I, Đukić A, Srejović I, Selaković D, Jakovljević V, Lukić ML. Transgenic Overexpression of Galectin-3 in Pancreatic β Cells Attenuates Hyperglycemia in Mice: Synergistic Antidiabetic Effect With Exogenous IL-33.. in 6th European Congress of Immunology; 2021 Sep 1-4; Virtual Meeting. 2021;:378.
doi:10.1002/eji.202170200 .

Jovičić, Nemanja, Petrović, Ivica, Pejnović, Nada, Ljujić, Biljana, Miletić Kovačević, Marina, Pavlović, Slađana, Jeftić, Ilija, Đukić, Aleksandar, Srejović, Ivan, Selaković, Dragica, Jakovljević, Vladimir, Lukić, Miodrag L., "Transgenic Overexpression of Galectin-3 in Pancreatic β Cells Attenuates Hyperglycemia in Mice: Synergistic Antidiabetic Effect With Exogenous IL-33." in 6th European Congress of Immunology; 2021 Sep 1-4; Virtual Meeting (2021):378,
https://doi.org/10.1002/eji.202170200 . .

TY  - GEN
AU  - Gazdić, Marina
AU  - Simović Marković, Bojana
AU  - Vučićević, Ljubica
AU  - Nikolić, Tamara
AU  - Đonov, Valentin
AU  - Arsenijević, Nebojša
AU  - Trajković, Vladimir
AU  - Lukić, Miodrag L.
AU  - Volarević, Vladislav
PY  - 2018
UR  - http://doi.wiley.com/10.1002/term.2452
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2833
AB  - The effects of mesenchymal stem cells (MSCs) on the phenotype and function of natural killer T (NKT) cells is not understood. We used concanavalin A (Con A) and α-galactosylceramide (α-GalCer)-induced liver injury to evaluate the effects of MSCs on NKT-dependent hepatotoxicity. Mouse MSCs (mMSCs) significantly reduced Con A- and α-GalCer-mediated hepatitis in C57Bl/6 mice, as demonstrated by histopathological and biochemical analysis, attenuated the influx of inflammatory [T-bet + , tumour necrosis factor-α (TNF-α), interferon-γ (IFN-γ)-producing and GATA3 + , interleukin-4 (IL-4)-producing] liver NKT cells and downregulated TNF-α, IFN-γ and IL-4 levels in the sera. The liver NKT cells cultured in vitro with mMSCs produced lower amounts of inflammatory cytokines (TNF-α, IFN-γ, IL-4) and higher amounts of immunosuppressive IL-10 upon α-GalCer stimulation. mMSC treatment attenuated expression of apoptosis-inducing ligands on liver NKT cells and suppressed the expression of pro-apoptotic genes in the livers of α-GalCer-treated mice. mMSCs reduced the cytotoxicity of liver NKT cells against hepatocytes in vitro. The presence of 1-methyl-dl-tryptophan, a specific inhibitor of indoleamine 2,3-dioxygenase (IDO), or l-N G -monomethyl arginine citrate, a specific inhibitor of inducible nitric oxide synthase (iNOS), in mMSC-conditioned medium injected into α-GalCer-treated mice, counteracted the hepatoprotective effect of mMSCs in vivo and restored pro-inflammatory cytokine production and cytotoxicity of NKT cells in vitro. Human MSCs attenuated the production of inflammatory cytokines in α-GalCer-stimulated human peripheral blood mononuclear cells in an iNOS- and IDO-dependent manner and reduced their cytotoxicity against HepG2 cells. In conclusion, MSCs protect from acute liver injury by attenuating the cytotoxicity and capacity of liver NKT cells to produce inflammatory cytokines in an iNOS- and IDO-dependent manner.
T2  - Journal of Tissue Engineering and Regenerative Medicine
T1  - Mesenchymal stem cells protect from acute liver injury by attenuating hepatotoxicity of liver natural killer T cells in an inducible nitric oxide synthase- and indoleamine 2,3-dioxygenase-dependent manner
IS  - 2
VL  - 12
DO  - 10.1002/term.2452
SP  - e1173
EP  - e1185
ER  - 

@misc{
author = "Gazdić, Marina and Simović Marković, Bojana and Vučićević, Ljubica and Nikolić, Tamara and Đonov, Valentin and Arsenijević, Nebojša and Trajković, Vladimir and Lukić, Miodrag L. and Volarević, Vladislav",
year = "2018",
abstract = "The effects of mesenchymal stem cells (MSCs) on the phenotype and function of natural killer T (NKT) cells is not understood. We used concanavalin A (Con A) and α-galactosylceramide (α-GalCer)-induced liver injury to evaluate the effects of MSCs on NKT-dependent hepatotoxicity. Mouse MSCs (mMSCs) significantly reduced Con A- and α-GalCer-mediated hepatitis in C57Bl/6 mice, as demonstrated by histopathological and biochemical analysis, attenuated the influx of inflammatory [T-bet + , tumour necrosis factor-α (TNF-α), interferon-γ (IFN-γ)-producing and GATA3 + , interleukin-4 (IL-4)-producing] liver NKT cells and downregulated TNF-α, IFN-γ and IL-4 levels in the sera. The liver NKT cells cultured in vitro with mMSCs produced lower amounts of inflammatory cytokines (TNF-α, IFN-γ, IL-4) and higher amounts of immunosuppressive IL-10 upon α-GalCer stimulation. mMSC treatment attenuated expression of apoptosis-inducing ligands on liver NKT cells and suppressed the expression of pro-apoptotic genes in the livers of α-GalCer-treated mice. mMSCs reduced the cytotoxicity of liver NKT cells against hepatocytes in vitro. The presence of 1-methyl-dl-tryptophan, a specific inhibitor of indoleamine 2,3-dioxygenase (IDO), or l-N G -monomethyl arginine citrate, a specific inhibitor of inducible nitric oxide synthase (iNOS), in mMSC-conditioned medium injected into α-GalCer-treated mice, counteracted the hepatoprotective effect of mMSCs in vivo and restored pro-inflammatory cytokine production and cytotoxicity of NKT cells in vitro. Human MSCs attenuated the production of inflammatory cytokines in α-GalCer-stimulated human peripheral blood mononuclear cells in an iNOS- and IDO-dependent manner and reduced their cytotoxicity against HepG2 cells. In conclusion, MSCs protect from acute liver injury by attenuating the cytotoxicity and capacity of liver NKT cells to produce inflammatory cytokines in an iNOS- and IDO-dependent manner.",
journal = "Journal of Tissue Engineering and Regenerative Medicine",
title = "Mesenchymal stem cells protect from acute liver injury by attenuating hepatotoxicity of liver natural killer T cells in an inducible nitric oxide synthase- and indoleamine 2,3-dioxygenase-dependent manner",
number = "2",
volume = "12",
doi = "10.1002/term.2452",
pages = "e1173-e1185"
}

Gazdić, M., Simović Marković, B., Vučićević, L., Nikolić, T., Đonov, V., Arsenijević, N., Trajković, V., Lukić, M. L.,& Volarević, V.. (2018). Mesenchymal stem cells protect from acute liver injury by attenuating hepatotoxicity of liver natural killer T cells in an inducible nitric oxide synthase- and indoleamine 2,3-dioxygenase-dependent manner. in Journal of Tissue Engineering and Regenerative Medicine, 12(2), e1173-e1185.
https://doi.org/10.1002/term.2452

Gazdić M, Simović Marković B, Vučićević L, Nikolić T, Đonov V, Arsenijević N, Trajković V, Lukić ML, Volarević V. Mesenchymal stem cells protect from acute liver injury by attenuating hepatotoxicity of liver natural killer T cells in an inducible nitric oxide synthase- and indoleamine 2,3-dioxygenase-dependent manner. in Journal of Tissue Engineering and Regenerative Medicine. 2018;12(2):e1173-e1185.
doi:10.1002/term.2452 .

Gazdić, Marina, Simović Marković, Bojana, Vučićević, Ljubica, Nikolić, Tamara, Đonov, Valentin, Arsenijević, Nebojša, Trajković, Vladimir, Lukić, Miodrag L., Volarević, Vladislav, "Mesenchymal stem cells protect from acute liver injury by attenuating hepatotoxicity of liver natural killer T cells in an inducible nitric oxide synthase- and indoleamine 2,3-dioxygenase-dependent manner" in Journal of Tissue Engineering and Regenerative Medicine, 12, no. 2 (2018):e1173-e1185,
https://doi.org/10.1002/term.2452 . .