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CXC chemokine ligand 12 protects pancreatic β-cells from necrosis through Akt kinase-mediated modulation of poly(ADP-ribose) polymerase-1 activity.

PloS one (2014-07-06)
Nevena Grdović, Svetlana Dinić, Mirjana Mihailović, Aleksandra Uskoković, Jelena Arambašić Jovanović, Goran Poznanović, Ludwig Wagner, Melita Vidaković
ABSTRACT

The diabetes prevention paradigm envisages the application of strategies that support the maintenance of appropriate β-cell numbers. Herein we show that overexpression of CXC chemokine ligand12 (CXCL12) considerably improves the viability of isolated rat Langerhans islet cells and Rin-5F pancreatic β-cells after hydrogen peroxide treatment. In rat islets and wt cells hydrogen peroxide treatment induced necrotic cell death that was mediated by the rapid and extensive activation of poly(ADP-ribose) polymerase-1 (PARP-1). In contrast, CXCL12-overexpressing cells were protected from necrotic cell death as a result of significantly reduced PARP-1 activity. CXCL12 downstream signalling through Akt kinase was responsible for the reduction of PARP-1 activity which switched cell death from necrosis to apoptosis, providing increased protection to cells from oxidative stress. Our results offer a novel aspect of the CXCL12-mediated improvement of β-cell viability which is based on its antinecrotic action through modulation of PARP-1 activity.

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