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dc.creatorVidaković, Melita
dc.creatorMihailović, Mirjana
dc.creatorSinadinović, Marija
dc.creatorRajić, Jovana
dc.creatorUskoković, Aleksandra
dc.creatorDinić, Svetlana
dc.creatorGrdović, Nevena
dc.creatorĐorđević, Miloš
dc.creatorTolić, Anja
dc.creatorPoznanović, Goran
dc.creatorCaballero, Garrido
dc.creatorArambašić Jovanović, Jelena
dc.date.accessioned2017-11-23T07:56:40Z
dc.date.available2017-11-23T07:56:40Z
dc.date.issued2017
dc.identifier.issn0354-4664
dc.identifier.urihttp://www.doiserbia.nb.rs/Article.aspx?ID=0354-46641700040V
dc.identifier.urihttps://ibiss-r.rcub.bg.ac.rs/handle/123456789/2886
dc.description.abstractWe 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.
dc.relationinfo:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/173020/RS//
dc.rightsopenAccess
dc.sourceArchives of Biological Sciences
dc.subjectDiabetes
dc.subjectCalcium
dc.subjectCXC chemokine ligand 12α
dc.subjectInsulin
dc.subjectPancreatic islet cells
dc.subjectVoltage-gated calcium channels
dc.titleCXC chemokine ligand 12α-mediated increase in insulin secretion and survival of mouse pancreatic islets in response to oxidative stress through modulation of calcium uptake
dc.typearticle
dc.rights.licenseBY-NC-ND
dcterms.abstractАрамбашић Јовановић, Јелена; Рајић, Јована; Видаковић, Мелита; Цабаллеро, Гарридо; Михаиловић, Мирјана; Синадиновић, Марија; Ускоковић, Александра; Динић, Светлана; Грдовић, Невена; Ђорђевић, Милош; Толић, Ања; Познановић, Горан
dc.rights.holder© Serbian Biological Society
dc.identifier.doi10.2298/ABS170711040V
dc.identifier.scopus2-s2.0-85043718185
dc.identifier.wos000428370100019
dc.citation.apaVidaković, M., Caballero, G., Mihailović, M., Arambašić-Jovanović, J., Sinadinović, M., Rajić, J., Uskoković, A., et al. (2017). 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, DOI:10.2298/ABS170711040V.
dc.citation.vancouverVidaković M, Caballero G, Mihailović M, Arambašić-Jovanović J, Sinadinović 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. Arch Biol Sci. 2017;DOI:10.2298/ABS170711040V.
dc.type.versionAccepted Version
dc.identifier.fulltexthttp://ibiss-r.rcub.bg.ac.rs/bitstream/id/79/bitstream_79.pdf
dc.citation.rankM23


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