Please use this identifier to cite or link to this item:
|Title:||Role of calcium independent phospholipase A2 in maintaining mitochondrial membrane potential and preventing excessive exocytosis in PC12 cells|
|Keywords:||Calcium independent phospholipase A2|
Mitochondrial membrane potential
Mitochondrial permeability transition pore
|Source:||Ma, M.-T.,Yeo, J.-F.,Farooqui, A.A.,Ong, W.-Y. (2011). Role of calcium independent phospholipase A2 in maintaining mitochondrial membrane potential and preventing excessive exocytosis in PC12 cells. Neurochemical Research 36 (2) : 347-354. ScholarBank@NUS Repository. https://doi.org/10.1007/s11064-010-0340-y|
|Abstract:||This study was carried out to elucidate the effects of calcium independent phospholipase A2 (iPLA2) on mitochondrial function and exocytosis in neuroendocrine cells. iPLA2 mRNA and protein were detected in cell lysates and mitochondria from PC12 cells. Treatment of cells with the iPLA2 inhibitor, bromoenol lactone (BEL), resulted in reduction in the mitochondrial membrane potential. Increase in membrane capacitance and number of spikes at amperometry, indicating exocytosis, were detected from PC12 cells after treatment with BEL. The induced exocytosis was abolished by pre-incubation of cells with the antioxidant, glutathione monoethyl ester, spin-trap/free radical scavenger, PBN, or inhibitors of the mitochondrial permeability transition pore, cyclosporine A and bongkrekic acid. These findings indicate that inhibition of iPLA2 results in excessive exocytosis through increased oxidative damage (or failure to repair such damage) and defects in mitochondrial function. A similar process may occur in neurons with mutations in iPLA2, leading to neuronal injury. © 2010 Springer Science+Business Media, LLC.|
|Source Title:||Neurochemical Research|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Dec 5, 2017
checked on Dec 8, 2017
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.