Cell Shrinkage is Essential in Lysophosphatidic Acid Signaling in Ehrlich Ascites Tumor Cells

Cell Shrinkage is Essential in Lysophosphatidic Acid Signaling in Ehrlich Ascites Tumor Cells The present study aimed at elucidating the initial intracellular lysophosphatidic acid (LPA)-induced signaling events, in order to investigate the sequence in which LPA affects the intracellular concentration of free, cytosolic Ca2+, [Ca2+] i , ion channels, the F-actin cytoskeleton, cell volume and the Na+/H+ exchanger. We found that stimulation of Ehrlich cells with LPA induced a transient, concentration-dependent increase in [Ca2+] i , which is due to Ca2+ release from intracellular Ins(1,4,5)P3-sensitive stores as well as an influx of Ca2+. The EC50 values for LPA-induced Ca2+ mobilization were estimated at 0.03 nm and 0.4 nm LPA in the presence and absence of extracellular Ca2+, respectively. The LPA-induced increase in [Ca2+] i resulted in (i) co-activation of Ca2+-activated, charybdotoxin (ChTX)-sensitive K+ and niflumic acid-sensitive Cl− currents; (ii) a subsequent cell shrinkage and increased polymerization of F-actin, and (iii) activation of a Na+/H+ exchange, resulting in a concentration-dependent intracellular alkalinization. The EC50 value for the LPA-induced rate of alkalinization was estimated at 0.37 nm LPA. When cell shrinkage was prevented, the LPA-induced activation of the Na+/H+ exchanger was impaired. In conclusion, the initial signaling events induced by LPA involves activation of volume regulatory mechanisms. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Membrane Biology Springer Journals

Cell Shrinkage is Essential in Lysophosphatidic Acid Signaling in Ehrlich Ascites Tumor Cells

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Publisher
Springer-Verlag
Copyright
Copyright © Inc. by 2000 Springer-Verlag New York
Subject
Life Sciences; Biochemistry, general; Human Physiology
ISSN
0022-2631
eISSN
1432-1424
D.O.I.
10.1007/s002320001003
Publisher site
See Article on Publisher Site

Abstract

The present study aimed at elucidating the initial intracellular lysophosphatidic acid (LPA)-induced signaling events, in order to investigate the sequence in which LPA affects the intracellular concentration of free, cytosolic Ca2+, [Ca2+] i , ion channels, the F-actin cytoskeleton, cell volume and the Na+/H+ exchanger. We found that stimulation of Ehrlich cells with LPA induced a transient, concentration-dependent increase in [Ca2+] i , which is due to Ca2+ release from intracellular Ins(1,4,5)P3-sensitive stores as well as an influx of Ca2+. The EC50 values for LPA-induced Ca2+ mobilization were estimated at 0.03 nm and 0.4 nm LPA in the presence and absence of extracellular Ca2+, respectively. The LPA-induced increase in [Ca2+] i resulted in (i) co-activation of Ca2+-activated, charybdotoxin (ChTX)-sensitive K+ and niflumic acid-sensitive Cl− currents; (ii) a subsequent cell shrinkage and increased polymerization of F-actin, and (iii) activation of a Na+/H+ exchange, resulting in a concentration-dependent intracellular alkalinization. The EC50 value for the LPA-induced rate of alkalinization was estimated at 0.37 nm LPA. When cell shrinkage was prevented, the LPA-induced activation of the Na+/H+ exchanger was impaired. In conclusion, the initial signaling events induced by LPA involves activation of volume regulatory mechanisms.

Journal

The Journal of Membrane BiologySpringer Journals

Published: Jan 1, 2000

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