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

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 CXCL1...

Full description

Bibliographic Details
Main Authors: Vidaković Melita, Caballero-Garrido Ernesto, Mihailović Mirjana, Arambašić-Jovanović Jelena, Sinadinović Marija, Rajić Jovana, Uskoković Aleksandra, Dinić Svetlana, Grdović Nevena, Đorđević Miloš, Tolić Anja, Poznanović Goran
Format: Article
Language:English
Published: University of Belgrade, University of Novi Sad 2018-01-01
Series:Archives of Biological Sciences
Subjects:
Online Access:http://www.doiserbia.nb.rs/img/doi/0354-4664/2018/0354-46641700040V.pdf
_version_ 1818498377877291008
author Vidaković Melita
Caballero-Garrido Ernesto
Mihailović Mirjana
Arambašić-Jovanović Jelena
Sinadinović Marija
Rajić Jovana
Uskoković Aleksandra
Dinić Svetlana
Grdović Nevena
Đorđević Miloš
Tolić Anja
Poznanović Goran
author_facet Vidaković Melita
Caballero-Garrido Ernesto
Mihailović Mirjana
Arambašić-Jovanović Jelena
Sinadinović Marija
Rajić Jovana
Uskoković Aleksandra
Dinić Svetlana
Grdović Nevena
Đorđević Miloš
Tolić Anja
Poznanović Goran
author_sort Vidaković Melita
collection DOAJ
description 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. [Project of the Serbian Ministry of Education, Science and Technological Development, Grant no. 173020]
first_indexed 2024-12-10T18:58:01Z
format Article
id doaj.art-1aa508f2027f469c9ee47d0ac02ec823
institution Directory Open Access Journal
issn 0354-4664
1821-4339
language English
last_indexed 2024-12-10T18:58:01Z
publishDate 2018-01-01
publisher University of Belgrade, University of Novi Sad
record_format Article
series Archives of Biological Sciences
spelling doaj.art-1aa508f2027f469c9ee47d0ac02ec8232022-12-22T01:37:05ZengUniversity of Belgrade, University of Novi SadArchives of Biological Sciences0354-46641821-43392018-01-0170119120410.2298/ABS170711040V0354-46641700040VCXC chemokine ligand 12α-mediated increase in insulin secretion and survival of mouse pancreatic islets in response to oxidative stress through modulation of calcium uptakeVidaković Melita0Caballero-Garrido Ernesto1Mihailović Mirjana2Arambašić-Jovanović Jelena3Sinadinović Marija4Rajić Jovana5Uskoković Aleksandra6Dinić Svetlana7Grdović Nevena8Đorđević Miloš9Tolić Anja10Poznanović Goran11Institute for Biological Research, Department of Molecular Biology, Belgrade + Universidad Miguel Hernández de Elche, Institute of Bioengineering, UNIT of Cell Physiology and Nutrition, Elche, SpainUniversidad Miguel Hernández de Elche, Institute of Bioengineering, UNIT of Cell Physiology and Nutrition, Elche, SpainInstitute for Biological Research, Department of Molecular Biology, BelgradeInstitute for Biological Research, Department of Molecular Biology, BelgradeInstitute for Biological Research, Department of Molecular Biology, BelgradeInstitute for Biological Research, Department of Molecular Biology, BelgradeInstitute for Biological Research, Department of Molecular Biology, BelgradeInstitute for Biological Research, Department of Molecular Biology, BelgradeInstitute for Biological Research, Department of Molecular Biology, BelgradeInstitute for Biological Research, Department of Molecular Biology, BelgradeInstitute for Biological Research, Department of Molecular Biology, BelgradeInstitute for Biological Research, Department of Molecular Biology, BelgradeWe 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. [Project of the Serbian Ministry of Education, Science and Technological Development, Grant no. 173020]http://www.doiserbia.nb.rs/img/doi/0354-4664/2018/0354-46641700040V.pdfdiabetescalciumCXC chemokine ligand 12αinsulinpancreatic islet cellsvoltage-gated calcium channels
spellingShingle Vidaković Melita
Caballero-Garrido Ernesto
Mihailović Mirjana
Arambašić-Jovanović Jelena
Sinadinović 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
Archives of Biological Sciences
diabetes
calcium
CXC chemokine ligand 12α
insulin
pancreatic islet cells
voltage-gated calcium channels
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
title_full 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
title_fullStr 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
title_full_unstemmed 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
title_short 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
title_sort 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
topic diabetes
calcium
CXC chemokine ligand 12α
insulin
pancreatic islet cells
voltage-gated calcium channels
url http://www.doiserbia.nb.rs/img/doi/0354-4664/2018/0354-46641700040V.pdf
work_keys_str_mv AT vidakovicmelita cxcchemokineligand12amediatedincreaseininsulinsecretionandsurvivalofmousepancreaticisletsinresponsetooxidativestressthroughmodulationofcalciumuptake
AT caballerogarridoernesto cxcchemokineligand12amediatedincreaseininsulinsecretionandsurvivalofmousepancreaticisletsinresponsetooxidativestressthroughmodulationofcalciumuptake
AT mihailovicmirjana cxcchemokineligand12amediatedincreaseininsulinsecretionandsurvivalofmousepancreaticisletsinresponsetooxidativestressthroughmodulationofcalciumuptake
AT arambasicjovanovicjelena cxcchemokineligand12amediatedincreaseininsulinsecretionandsurvivalofmousepancreaticisletsinresponsetooxidativestressthroughmodulationofcalciumuptake
AT sinadinovicmarija cxcchemokineligand12amediatedincreaseininsulinsecretionandsurvivalofmousepancreaticisletsinresponsetooxidativestressthroughmodulationofcalciumuptake
AT rajicjovana cxcchemokineligand12amediatedincreaseininsulinsecretionandsurvivalofmousepancreaticisletsinresponsetooxidativestressthroughmodulationofcalciumuptake
AT uskokovicaleksandra cxcchemokineligand12amediatedincreaseininsulinsecretionandsurvivalofmousepancreaticisletsinresponsetooxidativestressthroughmodulationofcalciumuptake
AT dinicsvetlana cxcchemokineligand12amediatedincreaseininsulinsecretionandsurvivalofmousepancreaticisletsinresponsetooxidativestressthroughmodulationofcalciumuptake
AT grdovicnevena cxcchemokineligand12amediatedincreaseininsulinsecretionandsurvivalofmousepancreaticisletsinresponsetooxidativestressthroughmodulationofcalciumuptake
AT đorđevicmilos cxcchemokineligand12amediatedincreaseininsulinsecretionandsurvivalofmousepancreaticisletsinresponsetooxidativestressthroughmodulationofcalciumuptake
AT tolicanja cxcchemokineligand12amediatedincreaseininsulinsecretionandsurvivalofmousepancreaticisletsinresponsetooxidativestressthroughmodulationofcalciumuptake
AT poznanovicgoran cxcchemokineligand12amediatedincreaseininsulinsecretionandsurvivalofmousepancreaticisletsinresponsetooxidativestressthroughmodulationofcalciumuptake