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6. Cell membrane potential oscillations induced by kinins in fibroblasts expressing the Ha-ras oncogene

Author

Lang F, Wöll E, Waldegger S, Friedrich F, Ritter M, Pinggera G, Karin Kloiber, Bichler I, Heitzenberger H, and Maly K

Subjects
Cell Membrane, 3T3 Cells, Fibroblasts, Bradykinin, Calcium Channel Blockers, Transfection, Membrane Potentials, Kinetics, Mice, Cell Transformation, Neoplastic, Genes, ras, Barium, Animals, Calcium
Abstract

In NIH-3T3 fibroblasts expressing the ras oncogene (+ras) bradykinin (BK) elicits sustained oscillations (1/min) of cell membrane potential (PD) due to oscillations of intracellular calcium activity with subsequent activation of calcium sensitive K+ channels. In NIH-3T3 fibroblasts not expressing the oncogene (-ras), BK leads to a single transient hyperpolarization of the cell membrane, not followed by oscillations. The oscillations of cell membrane potential require the presence of extracellular calcium and are abolished by K+ channel blocker barium (1 mmol/l), as well as by calcium channel blockers cadmium (1 mmol/l), lanthanum (0.1 mmol/l) and nifedipine (10 mumol/l). However, the oscillations are not modified by 1 mumol/l nifedipine, or by other calcium channel blockers, such as verapamil (10 mumol/l) or diltiazem (10 mumol/l). Cell proliferation is inhibited by nifedipine (10 mumol/l) but not by verapamil or diltiazem, indicating that the oscillations of intracellular calcium are a prerequisite for the growth factor independent proliferation of ras oncogene expressing cells.

8. Cell membrane potential oscillations induced by kinins in fibroblasts expressing the Ha-ras oncogene.

Author

Lang F, Wöll E, Waldegger S, Friedrich F, Ritter M, Pinggera G, Kloiber K, Bichler I, Heitzenberger H, and Maly K

Subjects
3T3 Cells, Animals, Barium pharmacology, Calcium pharmacology, Calcium Channel Blockers pharmacology, Cell Membrane drug effects, Fibroblasts physiology, Kinetics, Membrane Potentials drug effects, Mice, Transfection, Bradykinin pharmacology, Cell Membrane physiology, Cell Transformation, Neoplastic, Genes, ras
Abstract

In NIH-3T3 fibroblasts expressing the ras oncogene (+ras) bradykinin (BK) elicits sustained oscillations (1/min) of cell membrane potential (PD) due to oscillations of intracellular calcium activity with subsequent activation of calcium sensitive K+ channels. In NIH-3T3 fibroblasts not expressing the oncogene (-ras), BK leads to a single transient hyperpolarization of the cell membrane, not followed by oscillations. The oscillations of cell membrane potential require the presence of extracellular calcium and are abolished by K+ channel blocker barium (1 mmol/l), as well as by calcium channel blockers cadmium (1 mmol/l), lanthanum (0.1 mmol/l) and nifedipine (10 mumol/l). However, the oscillations are not modified by 1 mumol/l nifedipine, or by other calcium channel blockers, such as verapamil (10 mumol/l) or diltiazem (10 mumol/l). Cell proliferation is inhibited by nifedipine (10 mumol/l) but not by verapamil or diltiazem, indicating that the oscillations of intracellular calcium are a prerequisite for the growth factor independent proliferation of ras oncogene expressing cells.

Published
1992

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