Eur J Endocrinol
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DOI: 10.1530/eje.0.1460881
European Journal of Endocrinology, Vol 146, Issue 6, 881-889
Copyright © 2002 by European Society of Endocrinology
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Reduction of insulin secretion in the insulinoma cell line INS-1 by overexpression of a Ca(v)2.3 (alpha1E) calcium channel antisense cassette

A Pereverzev, R Vajna, G Pfitzer, J Hescheler, U Klockner, and T Schneider

Institute of Neurophysiology, University of Cologne, Robert Koch Strasse 39, D-50931 Cologne, Germany.

OBJECTIVE: Multiple types of voltage-activated Ca(2+) channels (T, L, N, P, Q and R type) coordinate a variety of Ca(2+)-dependent processes in neurons and neuroendocrine cells. In insulinoma cell lines as well as in endocrine tissues, the non-L-type alpha1E (Ca(v)2.3) subunit is expressed as the tissue-specific splice variant alpha1Ee. DESIGN AND METHODS: To understand the functional role of alpha1E-containing Ca(2+) channels, antisense alpha1E mRNA was overexpressed in INS-1 cells by stable transfection of an antisense alpha1E cassette cDNA. As controls, either a sense alpha1E cassette or a control vector containing enhanced green fluorescent protein as an unrelated gene was stably transfected. The overexpression of each transfected cassette cDNA was recorded by RT-PCR. RESULTS: In three independent antisense alpha1E INS-1 clones, the glucose-induced insulin release was significantly reduced as compared with wild-type INS-1 cells and with a sense alpha1E INS-1 clone. However, in the antisense INS-1 clones, the KCl-induced insulin release was less impaired by overexpressing the antisense alpha1E cassette than the glucose-induced insulin release, leading to the assumption that glucose (15 mmol/l) and KCl (25 mmol/l) finally depolarize the membrane potential to a different extent. CONCLUSION: alpha1E is involved in glucose-induced insulin secretion probably by influencing the excitability of INS-1 cells.


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