ERK activation by Ca2+ ionophores depends on Ca2+ entry in lymphocytes but not in platelets, and does not conduct membrane scrambling
Autor: | D. Kerbiriou-Nabias, Isabelle Garcin, I. Badirou, Jeanne Dachary-Prigent, D. Geldwerth-Feniger, A. Arachiche |
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Rok vydání: | 2008 |
Předmět: |
MAPK/ERK pathway
Blood Platelets Blotting Western Biology Jurkat cells Cellular and Molecular Neuroscience chemistry.chemical_compound Jurkat Cells Phospholipid scrambling Scott syndrome medicine Humans Lymphocytes Phosphorylation Extracellular Signal-Regulated MAP Kinases Molecular Biology Phospholipids Pharmacology Ionophores Kinase Cell Membrane Cell Biology Phosphatidylserine medicine.disease Flow Cytometry Cell biology chemistry Microscopy Fluorescence Cell culture Molecular Medicine Calcium Signal Transduction |
Zdroj: | Cellular and molecular life sciences : CMLS. 65(23) |
ISSN: | 1420-9071 |
Popis: | 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. |
Databáze: | OpenAIRE |
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