Abstract
We tracked lineage map of the Ins2 cells in mice and insulin expression in migration sites of cells. We studied effect of the Wnt/β-catenin signaling pathway on the migration. We studied insulin secretion status in submandibular gland of mice under hyperglycemia stress. Cre/loxp system was used to observe migration sites and timing of the Ins2-cre lineage cells. Immunohistochemistry and immunofluorescence was used to detecte presence of insulin in the Ins2-cre lineage cells. Knockout mice from E9.5 to adulthood was studied to explore role of the Wnt/β-catenin on the migration. Immunofluorescence and the QRT-PCR (Quantitative Real-time Polymerase Chain Reaction) was used to study insulin secretion in submandibular gland under hyperglycemic conditions. Expression sites of the Ins2-cre gene in adult mice decreased compared with postnatal mice, including the pancreas, tongue, submandibular, and brain. In the migration tissues of ins-cre cells, positive insulin expression was detected in the submandibular acinus, vessel element and pancreatic islets. In comparison to wild-type mice, Wnt/β-catenin signaling knockout mice displayed a slight rise of INS2 expression during the neonatal stage, with a notable increase in adulthood, particularly in areas near the oral cavity. Expression of insulin in submandibular gland of mice increased after 6 h of hyperglycemic stimulation (P < 0.05). Ins2 lineage cells can migrate to multiple organs in mice, where insulin may expressed. Inhibition or knockout of the Wnt/β-catenin signaling pathway may indirectly enhance the migratory capacity of INS2 cells. Submandibular glands may secrete insulin under stress of maintaining organismal homeostasis. Wnt/β-catenin may be the therapeutic target of diabetes. Submandibular glands may be a new target organ of gene therapy for diabetic patients.