Cell Swelling-induced Insulin Secretion from INS-1E Cells is Inhibited by Extracellular Ca2+ and is Tetanus Toxin Resistant

• Published in: Cellular physiology and biochemistry Vol. 26; no. 2; pp. 197 - 208
• Main Authors: Orečná, Martina, Hafko, Roman, Toporcerová, Veronika, Štrbák, Vladimír, Bačová, Zuzana
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland 01-01-2010
• Subjects: Animals; Calcium - pharmacology; Calcium Channel Blockers - pharmacology; Calcium Channels, L-Type - chemistry; Calcium Channels, L-Type - genetics; Calcium Channels, L-Type - metabolism; Calcium Channels, P-Type - chemistry; Calcium Channels, P-Type - genetics; Calcium Channels, P-Type - metabolism; Calcium Channels, Q-Type - chemistry; Calcium Channels, Q-Type - genetics; Calcium Channels, Q-Type - metabolism; Calcium Channels, R-Type - chemistry; Calcium Channels, R-Type - genetics; Calcium Channels, R-Type - metabolism; Calcium Channels, T-Type - chemistry; Calcium Channels, T-Type - genetics; Calcium Channels, T-Type - metabolism; Cell Line, Tumor; Cell Size; Egtazic Acid - analogs & derivatives; Egtazic Acid - pharmacology; Hypotonic Solutions - chemistry; Insulin - metabolism; Insulin Secretion; Male; Nifedipine - pharmacology; omega-Agatoxin IVA - pharmacology; Original Paper; Rats; SNARE Proteins - metabolism; SNARE Proteins - physiology; Tetanus Toxin - pharmacology; Tetanus toxin; Calcium channels; Ca2; SNARE; Insulin secretion; Cell swelling
• ISSN: 1015-8987; 1421-9778
• DOI: 10.1159/000320543

Cell swelling-induced insulin secretion represents an alternative pathway of stimulation of insulin secretion. INS-1E rat tumor beta cells do not release insulin in response to cell swelling in presence of Ca 2+ despite a good response to glucose challenge and appropriate increase in cell volume. Surprisingly, perifusion with Ca 2+ -depleted medium showed distinct secretory response of INS-1E cells to hypotonicity. Objective of this study was further characterization of the role of Ca 2+ in secretory process in INS-1 and INS-1E cell lines. Ca 2+ depleted hypotonic medium with 10 µM BAPTA/AM (intracellular chelator) induced insulin secretion from both types of cells. We demonstrated expression of L-type Ca 2+ channel Ca v 1.2 and non-L-type Ca 2+ channels Ca v 2.1 (P/Q-type), Ca v 2.2 (N-type), and Ca v 3.1 (T-type) in both cell lines. Inhibition of L type channel with nifedipine and/or P/Q type with ω-agatoxin IVA enabled distinct response to hypotonic medium also in INS-1E cells. Tetanus toxin (TeTx) in medium containing Ca 2+ and a group of calcium channel blockers inhibited hypotonicity-induced insulin secretion from INS-1 cells but not from INS-1E cells. Conclusion: Hypotonicity-induced insulin secretion from INS-1E cells is inhibited by extracellular Ca 2+ , does not require intracellular Ca 2+ and is TeTx resistant.