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Ca2+ ionophores trigger membrane remodeling without a need for store-operated Ca2+ entry
Marie Galitzine1, Thierry Capiod, Françoise Le Deist
1INSERM Unité 143, 80 rue du Général Leclerc, 94276, Le Kremlin-Bicêtre, France.
Biochemical and Biophysical Research Communications
|January 5, 2005
Summary
Calcium ionophores rapidly remodel cell membranes, exposing aminophospholipids for coagulation. This study reveals that this membrane remodeling occurs independently of store-operated calcium entry (SOCE).
Area of Science:
- Cell Biology
- Biochemistry
- Membrane Biophysics
Background:
- Calcium ionophores are potent agents for rapid in vitro membrane remodeling.
- This remodeling exposes aminophospholipids on blood cells, creating a catalytic surface for coagulation.
- The role of cytosolic calcium increase via store-operated calcium entry (SOCE) in ionophore-induced membrane remodeling is unclear.
Purpose of the Study:
- To investigate whether store-operated calcium entry (SOCE) is essential for ionophore-induced rapid membrane remodeling.
- To determine if ionophores trigger membrane remodeling independently of SOCE.
Main Methods:
- Utilized two mutant B lymphoblast cell lines with defective SOCE or altered membrane remodeling.
- Simultaneously assessed cytosolic calcium ion increase ([Ca2+]i) and membrane remodeling.
- Compared the effects of calcium ionophores and the Ca2+-ATPase inhibitor thapsigargin.
Main Results:
- Ionophores effectively induced rapid membrane remodeling in the studied cell lines.
- The presence of a functional SOCE pathway was not required for ionophore-mediated membrane remodeling.
- Thapsigargin elevated [Ca2+]i via SOCE but did not induce the same rapid membrane remodeling.
Conclusions:
- Ionophore-induced membrane remodeling occurs independently of store-operated calcium entry (SOCE).
- The findings differentiate the mechanisms of calcium ionophores and thapsigargin in cellular responses.
- This suggests distinct pathways mediate calcium influx and subsequent membrane changes.