The Journal of Neuroscience, September 13, 2006, ():
Regulation of Store-Operated Calcium Entry by Calcium-Independent Phospholipase A2 in Rat Cerebellar Astrocytes
J. Neurosci. Singaravelu et al.
26: 9579
Supplemental data
Files in this Data Supplement:
- supplemental material
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Supplimentary Figure 1: Hypothetical diagram of iPLA2-mediated SOCE in astrocytes. This diagram illustrates a model of SOCE in cerebellar astrocytes (Bergmann glia, GCL astrocytes) with respect to the approaches explored in this study. Inositol 1,4,5-triphosphate (IP3)-mediated Ca2+ release or the inhibition of SERCA-dependent Ca2+ refilling depletes Ca2+ stores of the endoplasmic reticulum (ER). After depletion of CPA-sensitive Ca2+ stores, an unknown factor released from ER, probably calcium influx factor (CIF), activates iPLA2 by removing the inhibitory calmodulin (CaM) complexed with iPLA2. The EF-hand protein STIM1, which migrates from the ER to the cell membrane upon store depletion could probably function as CIF. This results in the production of lysophospholipids and arachidonic acid (AA). The specific lysophospholipids, lysophosphatidylinositol (LPI) and lysophosphatidylcholine (LPC) activate 2-APB- and BTP2-sensitive SOCE channels in the plasma membrane, which leads to Ca2+ influx to refill the Ca2+ stores (ER), whereas AA opens 2-APB-insensitive, arachidonate-regulated Ca2+ channels. Inhibition of iPLA2 activity by specific antisense oligodeoxynucleotides of iPLA2 (AS-ODN), or by the iPLA2 blockers BEL and PACOCF3, reduces or suppresses SOCE. Ca2+ influx induced either by store depletion (CPA) or by CaM displacement (CMZ) are 2-APB-, BTP2- and BEL-sensitive. This suggests a key role of iPLA2 activity for activation of SOCE in astrocytes.
