[No authors listed]
Type 2 diabetes seriously affects human health and burdens public health systems. Pancreatic βâcell apoptosis contributes to a reduction in βâcell mass, which is responsible for the occurrence of type 2 diabetes. However, the mechanism that underlies this effect remains unclear. In the present study, the role of forkhead box O1 (Foxo1) was investigated (which is a key regulatory factor in βâcell function) in the apoptotic behavior of βâcells and a potential underlying mechanism was determined. It was demonstrated that Foxo1 overexpression significantly reduced the proliferation of INSâ1 cells and increased the apoptosis of INSâ1 cells, in contrast to foxm1, foxp, foxa1, foxc and foxb1 overexpression. The present study aimed to investigate potential underlying mechanisms using bioinformatics, including Gene Set and biological experiments, including flow cytometry, cell counting kitâ8, immunofluorescence, western blotting, reverse transcriptionâquantitative polymerase chain reaction analysis and lentiviral transfection. Further experiments conclusively showed that cluster of differentiation (CD)24 expression was significantly decreased when INSâ1 cells were treated with Foxo1. Animal experiments showed high CD24 expression in the pancreatic islets of diabetic GotoâKakizaki rats. Moreover, Gene Set showed that CD24 expression was associated with the adaptive immune response of βâcells. Finally, no significant differences in the proliferation and apoptosis of CD24 overexpressing INSâ1 cells were observed after Foxo1 treatment. These results suggested that Foxo1 overexpression in βâcells was able to increase apoptosis by inhibiting CD24 expression. This study may provide an approach for the treatment and prevention of type 2 diabetes.
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