2016/01/01 by Svetlana DINIĆ, Svetlana Dinić, Nevena GRDOVIĆ +13
Biochemistry, Genetics and Molecular Biology · Immunology and Microbiology · Medicine · #Calcium signaling and nucleotide metabolism #Immune Cell Function and Interaction #Pancreatic function and diabetes
paper · pdf · doi:10.2183/pjab.92.436
openalex publication_date 2016/01/01 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/22
Due to intrinsically low levels of antioxidant enzyme expression and activity, insulin producing pancreatic β-cells are particularly susceptible to free radical attack. In diabetes mellitus, which is accompanied by high levels of oxidative stress, this feature of β-cells significantly contributes to their damage and dysfunction. In light of the documented pro-survival effect of chemokine C-X-C Ligand 12 (CXCL12) on pancreatic β-cells, we examined its potential role in antioxidant protection. We report that CXCL12 overexpression enhanced the resistance of rat insulinoma (Rin-5F) and primary pancreatic islet cells to hydrogen peroxide (H2O2). CXCL12 lowered the levels of DNA damage and lipid peroxidation and preserved insulin expression. This effect was mediated through an increase in catalase (CAT) activity. By activating downstream p38, Akt and ERK kinases, CXCL12 facilitated Nrf2 nuclear translocation and enhanced its binding to the CAT gene promoter, inducing constitutive CAT expression and activity that was essential for protecting β-cells from H2O2.