INS2 lineage cell tracking and insulin expression in the related organs of mice.

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.