ERK activation by Ca2+ionophores depends on Ca2+entry in lymphocytes but not in platelets, and does not conduct membrane scrambling

被引:6
作者
Arachiche, A. [1 ,2 ,3 ,4 ]
Badirou, I. [1 ,2 ]
Dachary-Prigent, J. [3 ,4 ]
Garcin, I. [5 ]
Geldwerth-Feniger, D. [1 ,2 ]
Kerbiriou-Nabias, D. [1 ,2 ]
机构
[1] INSERM, U770, F-94276 Le Kremlin Bicetre, France
[2] Univ Paris Sud, F-94276 Le Kremlin Bicetre, France
[3] INSERM, U688, Bordeaux, France
[4] Univ Victor Segalen, Bordeaux, France
[5] Univ Paris 11, INSERM, UMR S757, F-91405 Orsay, France
关键词
Extracellular signal-regulated kinase; phosphatidylserine; phospholipid scrambling; platelet; Jurkat; B lymphocytes; Scott syndrome;
D O I
10.1007/s00018-008-8339-0
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
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.
引用
收藏
页码:3861 / 3871
页数:11
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