TY  - JOUR
AU  - Vidaković, Melita
AU  - Mihailović, Mirjana
AU  - Đorđević, Marija
AU  - Rajić, Jovana
AU  - Uskoković, Aleksandra
AU  - Dinić, Svetlana
AU  - Grdović, Nevena
AU  - Đorđević, Miloš
AU  - Tolić, Anja
AU  - Poznanović, Goran
AU  - Caballero, Garrido
AU  - Arambašić Jovanović, Jelena
PY  - 2018
UR  - http://www.doiserbia.nb.rs/Article.aspx?ID=0354-46641700040V
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2886
AB  - We examined whether CXCL12α improves insulin secretion by influencing the Ca2+ oscillation pattern and Ca2+ influx ([Ca2+]i), thereby enhancing the viability of pancreatic islet cells in oxidative stress. The islets of Langerhans were isolated from male OF1 mice and pretreated with 40 ng/mL of CXCL12α prior to exposure to 7.5 μM hydrogen peroxide, which served to induce oxidative stress. Incubation of islets with CXCL12α induced pancreatic β-cell proliferation and improved the ability of β-cells to withstand oxidative stress. Consecutive treatments of isolated islets with hydrogen peroxide caused a decline in β-cell functioning over time, while the CXCL12α pretreatment of islets exhibited a physiological response to high glucose that was comparable to control islets. The attenuated response of islets to a high D-glucose challenge was observed as a partial to complete abolishment of [Ca2+]i. Treatments with increasing concentrations of CXCL12α decreased the number of Ca2+ oscillations that lasted longer, thus pointing to an overall increase in [Ca2+]i, which was followed by increased insulin secretion. In addition, treatment of islets with CXCL12α enhanced the transcription rate for insulin and the CXCR4 gene, pointing to the importance of CXCL12/CXCR4 signaling in the regulation of Ca2+ intake and insulin secretion in pancreatic islet cells. We propose that a potential treatment with CXCL12α could help to remove preexisting glucotoxicity and associated temporary β-cell stunning that might be present at the time of diabetes diagnosis in vivo.
T2  - Archives of Biological Sciences
T1  - CXC chemokine ligand 12α-mediated increase in insulin secretion and survival of mouse pancreatic islets in response to oxidative stress through modulation of calcium uptake
IS  - 1
VL  - 70
DO  - 10.2298/ABS170711040V
SP  - 191
EP  - 204
ER  - 

@article{
author = "Vidaković, Melita and Mihailović, Mirjana and Đorđević, Marija and Rajić, Jovana and Uskoković, Aleksandra and Dinić, Svetlana and Grdović, Nevena and Đorđević, Miloš and Tolić, Anja and Poznanović, Goran and Caballero, Garrido and Arambašić Jovanović, Jelena",
year = "2018",
abstract = "We examined whether CXCL12α improves insulin secretion by influencing the Ca2+ oscillation pattern and Ca2+ influx ([Ca2+]i), thereby enhancing the viability of pancreatic islet cells in oxidative stress. The islets of Langerhans were isolated from male OF1 mice and pretreated with 40 ng/mL of CXCL12α prior to exposure to 7.5 μM hydrogen peroxide, which served to induce oxidative stress. Incubation of islets with CXCL12α induced pancreatic β-cell proliferation and improved the ability of β-cells to withstand oxidative stress. Consecutive treatments of isolated islets with hydrogen peroxide caused a decline in β-cell functioning over time, while the CXCL12α pretreatment of islets exhibited a physiological response to high glucose that was comparable to control islets. The attenuated response of islets to a high D-glucose challenge was observed as a partial to complete abolishment of [Ca2+]i. Treatments with increasing concentrations of CXCL12α decreased the number of Ca2+ oscillations that lasted longer, thus pointing to an overall increase in [Ca2+]i, which was followed by increased insulin secretion. In addition, treatment of islets with CXCL12α enhanced the transcription rate for insulin and the CXCR4 gene, pointing to the importance of CXCL12/CXCR4 signaling in the regulation of Ca2+ intake and insulin secretion in pancreatic islet cells. We propose that a potential treatment with CXCL12α could help to remove preexisting glucotoxicity and associated temporary β-cell stunning that might be present at the time of diabetes diagnosis in vivo.",
journal = "Archives of Biological Sciences",
title = "CXC chemokine ligand 12α-mediated increase in insulin secretion and survival of mouse pancreatic islets in response to oxidative stress through modulation of calcium uptake",
number = "1",
volume = "70",
doi = "10.2298/ABS170711040V",
pages = "191-204"
}

Vidaković, M., Mihailović, M., Đorđević, M., Rajić, J., Uskoković, A., Dinić, S., Grdović, N., Đorđević, M., Tolić, A., Poznanović, G., Caballero, G.,& Arambašić Jovanović, J.. (2018). CXC chemokine ligand 12α-mediated increase in insulin secretion and survival of mouse pancreatic islets in response to oxidative stress through modulation of calcium uptake. in Archives of Biological Sciences, 70(1), 191-204.
https://doi.org/10.2298/ABS170711040V

Vidaković M, Mihailović M, Đorđević M, Rajić J, Uskoković A, Dinić S, Grdović N, Đorđević M, Tolić A, Poznanović G, Caballero G, Arambašić Jovanović J. CXC chemokine ligand 12α-mediated increase in insulin secretion and survival of mouse pancreatic islets in response to oxidative stress through modulation of calcium uptake. in Archives of Biological Sciences. 2018;70(1):191-204.
doi:10.2298/ABS170711040V .

Vidaković, Melita, Mihailović, Mirjana, Đorđević, Marija, Rajić, Jovana, Uskoković, Aleksandra, Dinić, Svetlana, Grdović, Nevena, Đorđević, Miloš, Tolić, Anja, Poznanović, Goran, Caballero, Garrido, Arambašić Jovanović, Jelena, "CXC chemokine ligand 12α-mediated increase in insulin secretion and survival of mouse pancreatic islets in response to oxidative stress through modulation of calcium uptake" in Archives of Biological Sciences, 70, no. 1 (2018):191-204,
https://doi.org/10.2298/ABS170711040V . .

TY  - JOUR
AU  - Vidaković, Melita
AU  - Caballero, Garrido
AU  - Mihailović, Mirjana
AU  - Arambašić Jovanović, Jelena
AU  - Đorđević, Marija
AU  - Rajić, Jovana
AU  - Uskoković, Aleksandra
AU  - Dinić, Svetlana
AU  - Grdović, Nevena
AU  - Đorđević, Miloš
AU  - Tolić, Anja
AU  - Poznanović, Goran
PY  - 2018
UR  - http://www.doiserbia.nb.rs/Article.aspx?ID=0354-46641700040V
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3023
UR  - http://www.serbiosoc.org.rs/arch/index.php/abs/article/view/1940
AB  - We examined whether CXCL12α improves insulin secretion by influencing the Ca2+ oscillation pattern and Ca2+ influx ([Ca2+]i), thereby enhancing the viability of pancreatic islet cells in oxidative stress. The islets of Langerhans were isolated from male OF1 mice and pretreated with 40 ng/mL of CXCL12α prior to exposure to 7.5 μM hydrogen peroxide, which served to induce oxidative stress. Incubation of islets with CXCL12α induced pancreatic β-cell proliferation and improved the ability of β-cells to withstand oxidative stress. Consecutive treatments of isolated islets with hydrogen peroxide caused a decline in β-cell functioning over time, while the CXCL12α pretreatment of islets exhibited a physiological response to high glucose that was comparable to control islets. The attenuated response of islets to a high D-glucose challenge was observed as a partial to complete abolishment of [Ca2+]i. Treatments with increasing concentrations of CXCL12α decreased the number of Ca2+ oscillations that lasted longer, thus pointing to an overall increase in [Ca2+]i, which was followed by increased insulin secretion. In addition, treatment of islets with CXCL12α enhanced the transcription rate for insulin and the CXCR4 gene, pointing to the importance of CXCL12/CXCR4 signaling in the regulation of Ca2+ intake and insulin secretion in pancreatic islet cells. We propose that a potential treatment with CXCL12α could help to remove preexisting glucotoxicity and associated temporary β-cell stunning that might be present at the time of diabetes diagnosis in vivo.
PB  - Belgrade: Serbian Biological Society
T2  - Archives of Biological Sciences
T1  - CXC chemokine ligand 12α-mediated increase in insulin secretion and survival of mouse pancreatic islets in response to oxidative stress through modulation of calcium uptake
IS  - 1
VL  - 70
DO  - 10.2298/ABS170711040V
SP  - 191
EP  - 204
ER  - 

@article{
author = "Vidaković, Melita and Caballero, Garrido and Mihailović, Mirjana and Arambašić Jovanović, Jelena and Đorđević, Marija and Rajić, Jovana and Uskoković, Aleksandra and Dinić, Svetlana and Grdović, Nevena and Đorđević, Miloš and Tolić, Anja and Poznanović, Goran",
year = "2018",
abstract = "We examined whether CXCL12α improves insulin secretion by influencing the Ca2+ oscillation pattern and Ca2+ influx ([Ca2+]i), thereby enhancing the viability of pancreatic islet cells in oxidative stress. The islets of Langerhans were isolated from male OF1 mice and pretreated with 40 ng/mL of CXCL12α prior to exposure to 7.5 μM hydrogen peroxide, which served to induce oxidative stress. Incubation of islets with CXCL12α induced pancreatic β-cell proliferation and improved the ability of β-cells to withstand oxidative stress. Consecutive treatments of isolated islets with hydrogen peroxide caused a decline in β-cell functioning over time, while the CXCL12α pretreatment of islets exhibited a physiological response to high glucose that was comparable to control islets. The attenuated response of islets to a high D-glucose challenge was observed as a partial to complete abolishment of [Ca2+]i. Treatments with increasing concentrations of CXCL12α decreased the number of Ca2+ oscillations that lasted longer, thus pointing to an overall increase in [Ca2+]i, which was followed by increased insulin secretion. In addition, treatment of islets with CXCL12α enhanced the transcription rate for insulin and the CXCR4 gene, pointing to the importance of CXCL12/CXCR4 signaling in the regulation of Ca2+ intake and insulin secretion in pancreatic islet cells. We propose that a potential treatment with CXCL12α could help to remove preexisting glucotoxicity and associated temporary β-cell stunning that might be present at the time of diabetes diagnosis in vivo.",
publisher = "Belgrade: Serbian Biological Society",
journal = "Archives of Biological Sciences",
title = "CXC chemokine ligand 12α-mediated increase in insulin secretion and survival of mouse pancreatic islets in response to oxidative stress through modulation of calcium uptake",
number = "1",
volume = "70",
doi = "10.2298/ABS170711040V",
pages = "191-204"
}

Vidaković, M., Caballero, G., Mihailović, M., Arambašić Jovanović, J., Đorđević, M., Rajić, J., Uskoković, A., Dinić, S., Grdović, N., Đorđević, M., Tolić, A.,& Poznanović, G.. (2018). CXC chemokine ligand 12α-mediated increase in insulin secretion and survival of mouse pancreatic islets in response to oxidative stress through modulation of calcium uptake. in Archives of Biological Sciences
Belgrade: Serbian Biological Society., 70(1), 191-204.
https://doi.org/10.2298/ABS170711040V

Vidaković M, Caballero G, Mihailović M, Arambašić Jovanović J, Đorđević M, Rajić J, Uskoković A, Dinić S, Grdović N, Đorđević M, Tolić A, Poznanović G. CXC chemokine ligand 12α-mediated increase in insulin secretion and survival of mouse pancreatic islets in response to oxidative stress through modulation of calcium uptake. in Archives of Biological Sciences. 2018;70(1):191-204.
doi:10.2298/ABS170711040V .

Vidaković, Melita, Caballero, Garrido, Mihailović, Mirjana, Arambašić Jovanović, Jelena, Đorđević, Marija, Rajić, Jovana, Uskoković, Aleksandra, Dinić, Svetlana, Grdović, Nevena, Đorđević, Miloš, Tolić, Anja, Poznanović, Goran, "CXC chemokine ligand 12α-mediated increase in insulin secretion and survival of mouse pancreatic islets in response to oxidative stress through modulation of calcium uptake" in Archives of Biological Sciences, 70, no. 1 (2018):191-204,
https://doi.org/10.2298/ABS170711040V . .