Journal
CELLULAR AND MOLECULAR LIFE SCIENCES
Volume 65, Issue 23, Pages 3861-3871Publisher
SPRINGER BASEL AG
DOI: 10.1007/s00018-008-8339-0
Keywords
Extracellular signal-regulated kinase; phosphatidylserine; phospholipid scrambling; platelet; Jurkat; B lymphocytes; Scott syndrome
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Funding
- Nouvelle Societe Francaise d'Atherosclerose
- Fondation de France [2005 005347]
- INSERM
- Universite Paris-Sud (Le Kremlin-Bicetre)
- Universite Victor Segalen (Bordeaux)
- Fondation de France
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Rapid Ca2+- dependent phospholipid ( PL) reorganization ( scrambling) at the plasma membrane is a mechanism common to hematopoietic cells exposing procoagulant phosphatidylserine ( PS). The aim of this research was to determine whether activation of the extracellular signal- regulated kinase ( ERK) pathway was required for PL scrambling, based on a single report analyzing both responses induced by Ca2+ ionophores in megakaryoblastic HEL cells. Ca2+ ionophore- stimulated ERK phosphorylation was induced in platelets without external Ca2+, whereas exogenous Ca2+ entry was crucial for ERK activation in Jurkat T cells. In both cells, membrane scrambling only occurred following Ca2+ entry and was not blocked by inhibiting ERK phosphorylation. Furthermore, ERK proteins are strongly phosphorylated in transformed B lymphoblastic cell lines, which do not expose PS in their resting state. Overall, the data demonstrated that ERK activation and membrane scrambling are independent mechanisms.
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