Role of Calcium Independent Phospholipase A2 in Maintaining Mitochondrial Membrane Potential and Preventing Excessive Exocytosis in PC12 Cells

This study was carried out to elucidate the effects of calcium independent phospholipase A 2 (iPLA 2 ) on mitochondrial function and exocytosis in neuroendocrine cells. iPLA 2 mRNA and protein were detected in cell lysates and mitochondria from PC12 cells. Treatment of cells with the iPLA 2 inhibito...

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Bibliographic Details
Published in:Neurochemical research 2011-02, Vol.36 (2), p.347-354
Main Authors: Ma, May-Thu, Yeo, Jin-Fei, Farooqui, Akhlaq A., Ong, Wei-Yi
Format: Article
Language:English
Subjects:
Animals
Biochemistry
Biomedical and Life Sciences
Biomedicine
Cell Biology
Exocytosis - physiology
Isoenzymes - genetics
Isoenzymes - metabolism
Membrane Potential, Mitochondrial - physiology
Membrane Potentials - physiology
Mitochondria - metabolism
Naphthalenes - metabolism
Neurochemistry
Neurology
Neurosciences
Original Paper
PC12 Cells
Phosphodiesterase Inhibitors - metabolism
Phospholipases A2, Calcium-Independent - antagonists & inhibitors
Phospholipases A2, Calcium-Independent - genetics
Phospholipases A2, Calcium-Independent - metabolism
Pyrones - metabolism
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Summary:This study was carried out to elucidate the effects of calcium independent phospholipase A 2 (iPLA 2 ) on mitochondrial function and exocytosis in neuroendocrine cells. iPLA 2 mRNA and protein were detected in cell lysates and mitochondria from PC12 cells. Treatment of cells with the iPLA 2 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 iPLA 2 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 iPLA 2 , leading to neuronal injury.
ISSN:0364-3190
1573-6903
DOI:10.1007/s11064-010-0340-y