Role of extracellular signal-regulated kinase 1/2 signal transduction pathway in insulin secretion by β-TC6 cells

• Published in: Molecular medicine reports Vol. 13; no. 5; pp. 4451 - 4454
• Main Authors: NIU, BEN, LIU, LIJUAN, SU, HENG, XIA, XUESHAN, HE, QIU, FENG, YUE, XUE, YUANMING, YAN, XINMING
• Format: Journal Article
• Language: English
• Published: Greece D.A. Spandidos 01-05-2016; Spandidos Publications; Spandidos Publications UK Ltd
• Subjects: Animals; Apoptosis; Biotechnology; Cell Line; Cellular signal transduction; Diabetes; Enzyme inhibitors; Extracellular signal-regulated kinase; extracellular signal-regulated kinase 1/2 signal transduction pathway; Flavonoids - pharmacology; Genetic aspects; Glucose; Glucose - pharmacology; Health aspects; Insulin; Insulin - metabolism; Insulin resistance; Insulin Secretion; Kinases; MAP kinase; MAP Kinase Signaling System - drug effects; MAP Kinase Signaling System - physiology; Mice; Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors; Mitogen-Activated Protein Kinase 3 - metabolism; Pancreas; Pancreas - cytology; Pancreas - metabolism; Pancreatic beta cells; Phosphorylation; Phosphorylation - drug effects; Phosphorylation - physiology; Phosphotransferases; Properties; Protein kinase; Proteins; Radioimmunoassay; Rodents; Secretion; Signal transduction; Statistical analysis; β-TC6; Beijing China; United States > US; China
• ISSN: 1791-2997; 1791-3004
• DOI: 10.3892/mmr.2016.5053

The present study aimed to investigate the role of the extracellular signal-regulated kinase (ERK)1/2 signal transduction pathway in glucose-stimulated insulin secretion in β-TC6 mouse pancreatic cells. Insulin production by β-TC6 cells was stimulated with various concentrations of glucose, which was dose-dependently inhibited by mitogen-activated protein kinase inhibitor PD98059, as indicated by a radioimmunoassay. Furthermore, glucose stimulation enhanced the phosphorylation of ERK1/2, which was dose-dependently inhibited by PD98059, as indicated by western blot analysis. These results indicated that the activation of the ERK1/2 signal transduction pathway may have an important role in glucose-stimulated insulin secretion in β-TC6 cells.