Ca 2+ entry through reverse Na + /Ca 2+ exchanger in NCI-H716, glucagon-like peptide-1 secreting cells

• Published in: The Korean journal of physiology & pharmacology Vol. 26; no. 3; pp. 219 - 225
• Main Authors: Choi, Kyung Jin, Hwang, Jin Wook, Kim, Se Hoon, Park, Hyung Seo
• Format: Journal Article
• Language: Korean
• Published: 2022
• Subjects: Calcium entry; Carbamylcholine; NCI-H716; Na^+/Ca^{2+}$ exchanger; Glucagon like peptide-1
• ISSN: 1226-4512; 2093-3827

Glucagon like peptide-1 (GLP-1) released from enteroendocine L-cells in the intestine has incretin effects due to its ability to amplify glucose-dependent insulin secretion. Promotion of an endogenous release of GLP-1 is one of therapeutic targets for type 2 diabetes mellitus. Although the secretion of GLP-1 in response to nutrient or neural stimuli can be triggered by cytosolic Ca2+ elevation, the stimulus-secretion pathway is not completely understood yet. Therefore, the aim of this study was to investigate the role of reverse Na+/Ca2+ exchanger (rNCX) in Ca2+ entry induced by muscarinic stimulation in NCI-H716 cells, a human enteroendocrine GLP-1 secreting cell line. Intracellular Ca2+ was repetitively oscillated by the perfusion of carbamylcholine (CCh), a muscarinic agonist. The oscillation of cytosolic Ca2+ was ceased by substituting extracellular Na+ with Li+ or NMG+. KB-R7943, a specific rNCX blocker, completely diminished CCh-induced cytosolic Ca2+ oscillation. Type 1 Na+/Ca2+ exchanger (NCX1) proteins were expressed in NCI-H716 cells. These results suggest that rNCX might play a crucial role in Ca2+ entry induced by cholinergic stimulation in NCI-H716 cells, a GLP-1 secreting cell line.