Cell swelling-induced insulin secretion from INS-1E cells is inhibited by extracellular Ca2+ and is tetanus toxin resistant.
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 muM 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 omega-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.


CONCLUSIONS
Hypotonicity-induced insulin secretion from INS-1E cells is inhibited by extracellular Ca(2+), does not require intracellular Ca(2+) and is TeTx resistant.
Orecná
Martina
M
Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava, Slovakia.
Hafko
Roman
R
Toporcerová
Veronika
V
Strbák
Vladimír
V
Bacová
Zuzana
Z
D000818:Animals; D002118:Calcium / Q000494:pharmacology*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020746:Calcium Channels, L-Type / Q000737:chemistry / Q000235:genetics / Q000378:metabolism; D020865:Calcium Channels, P-Type / Q000737:chemistry / Q000235:genetics / Q000378:metabolism; D020907:Calcium Channels, Q-Type / Q000737:chemistry / Q000235:genetics / Q000378:metabolism; D020908:Calcium Channels, R-Type / Q000737:chemistry / Q000235:genetics / Q000378:metabolism; D020747:Calcium Channels, T-Type / Q000737:chemistry / Q000235:genetics / Q000378:metabolism; D045744:Cell Line, Tumor; D048429:Cell Size; D004533:Egtazic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D007038:Hypotonic Solutions / Q000737:chemistry; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D008297:Male; D009543:Nifedipine / Q000494:pharmacology; D051381:Rats; D050600:SNARE Proteins / Q000378:metabolism / Q000502:physiology; D013744:Tetanus Toxin / Q000494:pharmacology*; D020867:omega-Agatoxin IVA / Q000494:pharmacology
D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; D020865:Calcium Channels, P-Type; D020907:Calcium Channels, Q-Type; D020908:Calcium Channels, R-Type; D020747:Calcium Channels, T-Type; D007038:Hypotonic Solutions; D007328:Insulin; D050600:SNARE Proteins; D013744:Tetanus Toxin; D020867:omega-Agatoxin IVA; C070379:1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester; D004533:Egtazic Acid; D009543:Nifedipine; D002118:Calcium