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|Title:||Kainate receptors mediate regulated exocytosis of secretory phospholipase A2 in SH-SY5Y neuroblastoma cells||Authors:||Farooqui, Akhlaq A.
|Keywords:||DRNTU::Science::Biological sciences::Human anatomy and physiology::Neurobiology||Issue Date:||2011||Source:||Than, A., Tan, Y., Ong, W. Y., Farooqui, A. A., & Chen P. (2012). Kainate Receptors Mediate Regulated Exocytosis of Secretory Phospholipase A2 in SH-SY5Y Neuroblastoma Cells. Neurosignals, 20(2), 72-85.||Series/Report no.:||Neurosignals||Abstract:||Secretory phospholipase A(2) (sPLA(2)) isoforms are widely expressed in the brain and spinal cord. Group IIA sPLA(2) (sPLA(2)-IIA) has been shown to stimulate exocytosis and release of neurotransmitters in neuroendocrine PC12 cells and neurons, suggesting a role of the enzyme in neuronal signaling and synaptic transmission. However, the mechanisms by which sPLA(2) is itself released, and a possible relation between glutamate receptors and sPLA(2) exocytosis, are unknown. This study was carried out to elucidate the effects of glutamate receptor agonists on exocytosis of sPLA(2)-IIA in transfected SH-SY5Y neuroblastoma cells. sPLA(2)-IIA enzyme was packaged in fusion-competent vesicles and released constitutively or upon stimulation, suggesting regulated secretion. The signal peptide of sPLA(2)-IIA is required for its vesicular localization and exocytosis. External application of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainate (KA) induced vesicular exocytosis and release of sPLA(2)-IIA. UBP 302, a GluR5-specific KA receptor antagonist, abolished the effect of KA, confirming the role of KA receptors in mediating sPLA(2)-IIA secretion. Moreover, KA-induced sPLA(2)-IIA secretion is dependent on Ca(2+) and protein kinase C. Together, these findings provide evidence of a link between glutamate receptors and regulated sPLA(2) secretion in neurons that may play an important role in synaptic plasticity, pain transmission and neurodegenerative diseases.||URI:||https://hdl.handle.net/10356/107467
|DOI:||http://dx.doi.org/10.1159/000330414||Rights:||© 2011 S. Karger AG, Basel.||Fulltext Permission:||open||Fulltext Availability:||With Fulltext|
|Appears in Collections:||SCBE Journal Articles|
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