Objective: To investigate the effect of vascular endothelial growth factor (VEGF) on proliferation, apoptosis, insulin secretion and related gene expression in rat pancreatic islet cell (INS-1).

Methods: INS-1 cells were treated with different concentrations of VEGF. CCK-8 kit was used to detect the proliferation of INS-1 cells and the cell apoptosis were evaluated by using Annexin V and propidium iodide (PI) double staining kit. INS-1 cells were treated with VEGF and the standard glucose stimulated insulin secretion test with ELISA was conducted. The expression of related genes in pancreatic islets was detected by real-time quantitative PCR. The effect of VEGF on isulin protein expression was evaluated with Western blot.

Results: No significant changes (P > 0.05) in INS-1 cells were observed after treated with different concentrations of VEGF at 24 h, 48 h and 72 h. But when VEGF concentration were 80 ng/mL and 160 ng/mL, an inhibitory effect on cell apoptosis were noticed (P < 0.01). The addition of VEGF to the high-glucose media significantly reduced the release of insulin at the concentration of 40 ng/mL. A decreasing trends of the expression level of sulfonylurea receptor gene (Sur), inwardly rectifying potassium channel gene 6. 2 (Kir6. 2) as well as the release of insulin were noticed as the increasing of VEGF concentrations. The expression of glucokinase gene (GCK) first decreased and then increased, but the expression of glucose transporter gene 2 (Glut 2) were increased first and then decreased. CONCLUSION; VEGF inhibited the secretion of insulin from INS-1 cells in the high-glucose condition. Our study provides new clues to the function of VEGF on the glucose metabolism.

Download full-text PDF

Source

Publication Analysis

Top Keywords

ins-1 cells
20
insulin secretion
12
vegf
10
vegf proliferation
8
proliferation apoptosis
8
apoptosis insulin
8
rat pancreatic
8
pancreatic islet
8
cells treated
8
treated concentrations
8

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!