Relation between phosphatidylserine exposure and store-operated Ca(2+) entry in stimulated cells

A significant increase in intracellular Ca(2+) is required to trigger the remodeling of the cell plasma membrane. Scott syndrome is an extremely rare inherited disorder of the transmembrane migration of phosphatidylserine toward the exoplasmic leaflet in blood cells. We have recently reported a redu...

Full description

Saved in:
Bibliographic Details
Published in:Biochemical and biophysical research communications 2000-12, Vol.279 (2), p.639-645
Main Authors: Martin, S, Laude-Lemaire, I, Kerbiriou-Nabias, D, Freyssinet, J M, Martínez, M C
Format: Article
Language:English
Subjects:
Aged
B-Lymphocytes - drug effects
B-Lymphocytes - physiology
Blood Coagulation Disorders - blood
Blood Coagulation Disorders - genetics
Caffeine - pharmacology
Calcimycin - pharmacology
Calcium - blood
Calcium Signaling - drug effects
Calcium Signaling - physiology
Cell Membrane - drug effects
Cell Membrane - physiology
Cells, Cultured
Egtazic Acid - pharmacology
Female
Hemorrhage - etiology
Herpesvirus 4, Human - physiology
Humans
phosphatidylserine
Phosphatidylserines - blood
Reference Values
Syndrome
Thapsigargin - pharmacology
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:A significant increase in intracellular Ca(2+) is required to trigger the remodeling of the cell plasma membrane. Scott syndrome is an extremely rare inherited disorder of the transmembrane migration of phosphatidylserine toward the exoplasmic leaflet in blood cells. We have recently reported a reduced capacitative Ca(2+) entry in Scott cells [Martínez et al. (1999) Biochemistry 38, 10092-10098]. We have investigated here the links between defective phosphatidylserine exposure and Ca(2+) signaling in Scott cells by focusing on the Ca(2+) entry following the emptying of intracellular stores. After depletion of caffeine- or thapsigargin-sensitive stores, Ca(2+) entry was lower in Scott compared to control lymphoblasts. However, the simultaneous depletion of both types of stores restored a normal Ca(2+) influx across the plasma membrane in Scott cells and phosphatidylserine externalization ability was improved concomitantly with capacitative Ca(2+) entry. These observations point to the essential role of capacitative Ca(2+) entry in the control of phosphatidylserine exposure of stimulated cells.
ISSN:0006-291X
DOI:10.1006/bbrc.2000.3980