Tetraspanin-2 promotes glucotoxic apoptosis by regulating JNK/β-catenin signaling pathway in human pancreatic β-cells. Homo sapiens

Diabetes mellitus is a complex and heterogeneous disease that has β cell dysfunction at its core. Glucose toxicity affects pancreatic islets where it leads to β cell apoptosis. However, the role of JNK/β-catenin signaling pathway in glucotoxic β-cell apoptosis is poorly understood. To identify the potential genes whose expression changed in response to high glucose, we performed microarray analysis of gene expression in the RNAKT-15 cells for 48 h. Among the 41,000 genes tested, 1394 and 741 were twofold-upregulated and -downregulated, respectively. Genes involved in carbohydrate metabolism, cell cycle control, apoptotic process, and response to reactive oxygen species were upregulated. In contrast, genes involved in intracellular protein traffic, cell cycle, cell adhesion-mediated signaling, cell cycle control, response to reactive oxygen species, and apoptotic process were downregulated under high glucose-treated RNAKT-15 cells. Overall design: RNAKT-15 cells were incubated with low glucose (5mM, LC), and high glucose (33mM, HC) for 48 hours. The microarray experiments were performed in triplicate.