TY  - JOUR
AU  - Nikolić, Sandra
AU  - Gazdić-Janković, Marina
AU  - Rosić, Gvozden
AU  - Miletić-Kovačević, Marina
AU  - Jovičić, Nemanja
AU  - Nestorović, Nataša
AU  - Stojković, Petra
AU  - Filipović, Nenad
AU  - Milošević-Đorđević, Olivera
AU  - Selaković, Dragica
AU  - Živanović, Marko
AU  - Seklić, Dragana
AU  - Milivojević, Nevena
AU  - Marković, Aleksandra
AU  - Seist, Richard
AU  - Vasilijić, Sasa
AU  - Stanković, Konstantina M.
AU  - Stojković, Miodrag
AU  - Ljujić, Biljana
PY  - 2022
UR  - http://www.ncbi.nlm.nih.gov/pubmed/35405220
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/4950
AB  - Commercially manufactured or generated through environmental degradation, microplastics (MPs) and nanoplastics (NPs) considerably contribute to environmental pollution. There is a knowledge gap in how exposure to MPs/NPs changes cellular function and affects animal and human health. Here, we demonstrate that after oral uptake, fluorescent polystyrene (PS) nanoparticles pass through the mouse digestive system, accumulate and aggregate in different organs, and induce functional changes in cells and organs. Using cochlear explant as a novel in vitro system, we confirmed the consequences of PS-MP/NP interaction with inner ear cells by detecting aggregates and hetero-aggregates of PS particles in hair cells. The testes of treated males accumulated MPs/NPs in the interstitial compartment surrounding the seminiferous tubules, which was associated with a statistically significant decrease in testosterone levels. Male mice showed increased secretion of interleukins (IL-12p35 and IL-23) by splenocytes while cyto- and genotoxicity tests indicated impaired cell viability and increased DNA damage in spleen tissue. Males also showed a broad range of anxiogenic responses to PS nanoparticles while hippocampal samples from treated females showed an increased expression of Bax and Nlrp3 genes, indicating a pro-apoptotic/proinflammatory effect of PS treatment. Taken together, induced PS effects are also gender-dependent, and therefore, strongly motivate future research to mitigate the deleterious effects of nanosized plastic particles.
PB  - Elsevier Ltd
T2  - Environmental Pollution
T1  - Orally administered fluorescent nanosized polystyrene particles affect cell viability, hormonal and inflammatory profile, and behavior in treated mice.
VL  - 305
DO  - 10.1016/j.envpol.2022.119206
SP  - 119206
ER  - 

@article{
author = "Nikolić, Sandra and Gazdić-Janković, Marina and Rosić, Gvozden and Miletić-Kovačević, Marina and Jovičić, Nemanja and Nestorović, Nataša and Stojković, Petra and Filipović, Nenad and Milošević-Đorđević, Olivera and Selaković, Dragica and Živanović, Marko and Seklić, Dragana and Milivojević, Nevena and Marković, Aleksandra and Seist, Richard and Vasilijić, Sasa and Stanković, Konstantina M. and Stojković, Miodrag and Ljujić, Biljana",
year = "2022",
abstract = "Commercially manufactured or generated through environmental degradation, microplastics (MPs) and nanoplastics (NPs) considerably contribute to environmental pollution. There is a knowledge gap in how exposure to MPs/NPs changes cellular function and affects animal and human health. Here, we demonstrate that after oral uptake, fluorescent polystyrene (PS) nanoparticles pass through the mouse digestive system, accumulate and aggregate in different organs, and induce functional changes in cells and organs. Using cochlear explant as a novel in vitro system, we confirmed the consequences of PS-MP/NP interaction with inner ear cells by detecting aggregates and hetero-aggregates of PS particles in hair cells. The testes of treated males accumulated MPs/NPs in the interstitial compartment surrounding the seminiferous tubules, which was associated with a statistically significant decrease in testosterone levels. Male mice showed increased secretion of interleukins (IL-12p35 and IL-23) by splenocytes while cyto- and genotoxicity tests indicated impaired cell viability and increased DNA damage in spleen tissue. Males also showed a broad range of anxiogenic responses to PS nanoparticles while hippocampal samples from treated females showed an increased expression of Bax and Nlrp3 genes, indicating a pro-apoptotic/proinflammatory effect of PS treatment. Taken together, induced PS effects are also gender-dependent, and therefore, strongly motivate future research to mitigate the deleterious effects of nanosized plastic particles.",
publisher = "Elsevier Ltd",
journal = "Environmental Pollution",
title = "Orally administered fluorescent nanosized polystyrene particles affect cell viability, hormonal and inflammatory profile, and behavior in treated mice.",
volume = "305",
doi = "10.1016/j.envpol.2022.119206",
pages = "119206"
}

Nikolić, S., Gazdić-Janković, M., Rosić, G., Miletić-Kovačević, M., Jovičić, N., Nestorović, N., Stojković, P., Filipović, N., Milošević-Đorđević, O., Selaković, D., Živanović, M., Seklić, D., Milivojević, N., Marković, A., Seist, R., Vasilijić, S., Stanković, K. M., Stojković, M.,& Ljujić, B.. (2022). Orally administered fluorescent nanosized polystyrene particles affect cell viability, hormonal and inflammatory profile, and behavior in treated mice.. in Environmental Pollution
Elsevier Ltd., 305, 119206.
https://doi.org/10.1016/j.envpol.2022.119206

Nikolić S, Gazdić-Janković M, Rosić G, Miletić-Kovačević M, Jovičić N, Nestorović N, Stojković P, Filipović N, Milošević-Đorđević O, Selaković D, Živanović M, Seklić D, Milivojević N, Marković A, Seist R, Vasilijić S, Stanković KM, Stojković M, Ljujić B. Orally administered fluorescent nanosized polystyrene particles affect cell viability, hormonal and inflammatory profile, and behavior in treated mice.. in Environmental Pollution. 2022;305:119206.
doi:10.1016/j.envpol.2022.119206 .

Nikolić, Sandra, Gazdić-Janković, Marina, Rosić, Gvozden, Miletić-Kovačević, Marina, Jovičić, Nemanja, Nestorović, Nataša, Stojković, Petra, Filipović, Nenad, Milošević-Đorđević, Olivera, Selaković, Dragica, Živanović, Marko, Seklić, Dragana, Milivojević, Nevena, Marković, Aleksandra, Seist, Richard, Vasilijić, Sasa, Stanković, Konstantina M., Stojković, Miodrag, Ljujić, Biljana, "Orally administered fluorescent nanosized polystyrene particles affect cell viability, hormonal and inflammatory profile, and behavior in treated mice." in Environmental Pollution, 305 (2022):119206,
https://doi.org/10.1016/j.envpol.2022.119206 . .

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  - JOUR
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  - Jakovljević, Vladimir
AU  - Lukić, Miodrag L.
PY  - 2021
UR  - https://www.frontiersin.org/articles/10.3389/fphar.2021.714683/full
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/4697
AB  - Galectin-3 (Gal-3) has diverse roles in inflammatory and autoimmune diseases. There is evidence that Gal-3 plays a role in both type 1 and type 2 diabetes. While the role of Gal-3 expression in immune cells invading the pancreatic islets in the experimental model of type 1 diabetes mellitus has been already studied, the importance of the overexpression of Gal-3 in the target β cells is not defined. Therefore, we used multiple low doses of streptozotocin (MLD-STZ)-induced diabetes in C57Bl/6 mice to analyze the effect of transgenic (TG) overexpression of Gal-3 in β cells. Our results demonstrated that 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 pro-inflammatory cells without affecting the presence of T-regulatory cells. As the application of exogenous interleukin 33 (IL-33) given from the beginning of MLD-STZ diabetes induction attenuates the development of disease, by increasing the presence of regulatory FoxP3+ ST2+ cells, we evaluated the potential synergistic effect of the exogenous IL-33 and TG overexpression of Gal-3 in β cells at the later stage of diabetogenesis. The addition of IL-33 potentiated the survival of β cells and attenuated diabetes even when administered later, after the onset of hyperglycemia (12-18 days), suggesting that protection from apoptosis and immunoregulation by IL-33 may attenuate type 1 diabetes.
PB  - Lausanne: Frontiers Media S.A.
T2  - Frontiers in Pharmacology
T1  - Transgenic Overexpression of Galectin-3 in Pancreatic β Cells Attenuates Hyperglycemia in Mice: Synergistic Antidiabetic Effect With Exogenous IL-33.
VL  - 12
DO  - 10.3389/fphar.2021.714683
SP  - 714683
ER  - 

@article{
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 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 Gal-3 plays a role in both type 1 and type 2 diabetes. While the role of Gal-3 expression in immune cells invading the pancreatic islets in the experimental model of type 1 diabetes mellitus has been already studied, the importance of the overexpression of Gal-3 in the target β cells is not defined. Therefore, we used multiple low doses of streptozotocin (MLD-STZ)-induced diabetes in C57Bl/6 mice to analyze the effect of transgenic (TG) overexpression of Gal-3 in β cells. Our results demonstrated that 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 pro-inflammatory cells without affecting the presence of T-regulatory cells. As the application of exogenous interleukin 33 (IL-33) given from the beginning of MLD-STZ diabetes induction attenuates the development of disease, by increasing the presence of regulatory FoxP3+ ST2+ cells, we evaluated the potential synergistic effect of the exogenous IL-33 and TG overexpression of Gal-3 in β cells at the later stage of diabetogenesis. The addition of IL-33 potentiated the survival of β cells and attenuated diabetes even when administered later, after the onset of hyperglycemia (12-18 days), suggesting that protection from apoptosis and immunoregulation by IL-33 may attenuate type 1 diabetes.",
publisher = "Lausanne: Frontiers Media S.A.",
journal = "Frontiers in Pharmacology",
title = "Transgenic Overexpression of Galectin-3 in Pancreatic β Cells Attenuates Hyperglycemia in Mice: Synergistic Antidiabetic Effect With Exogenous IL-33.",
volume = "12",
doi = "10.3389/fphar.2021.714683",
pages = "714683"
}

Jovičić, N., Petrović, I., Pejnović, N., Ljujić, B., Miletić Kovačević, M., Pavlović, S., Jeftić, I., Đukić, A., Srejović, I., 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 Frontiers in Pharmacology
Lausanne: Frontiers Media S.A.., 12, 714683.
https://doi.org/10.3389/fphar.2021.714683

Jovičić N, Petrović I, Pejnović N, Ljujić B, Miletić Kovačević M, Pavlović S, Jeftić I, Đukić A, Srejović I, 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 Frontiers in Pharmacology. 2021;12:714683.
doi:10.3389/fphar.2021.714683 .

Jovičić, Nemanja, Petrović, Ivica, Pejnović, Nada, Ljujić, Biljana, Miletić Kovačević, Marina, Pavlović, Slađana, Jeftić, Ilija, Đukić, Aleksandar, Srejović, Ivan, 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 Frontiers in Pharmacology, 12 (2021):714683,
https://doi.org/10.3389/fphar.2021.714683 . .

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 . .