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 . .