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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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| Published in: | Neurochemical research 2011-02, Vol.36 (2), p.347-354 |
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| Main Authors: | , , , |
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| Language: | English |
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| cites | cdi_FETCH-LOGICAL-c258y-c1a69dcda0d1429acce8bb3b703d8905d5d118f9c251f1f7df510c3d3f5e95303 |
| container_end_page | 354 |
| container_issue | 2 |
| container_start_page | 347 |
| container_title | Neurochemical research |
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| creator | Ma, May-Thu Yeo, Jin-Fei Farooqui, Akhlaq A. Ong, Wei-Yi |
| description | 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. |
| doi_str_mv | 10.1007/s11064-010-0340-y |
| format | article |
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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.</description><identifier>ISSN: 0364-3190</identifier><identifier>EISSN: 1573-6903</identifier><identifier>DOI: 10.1007/s11064-010-0340-y</identifier><identifier>PMID: 21116712</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>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 ; Rats</subject><ispartof>Neurochemical research, 2011-02, Vol.36 (2), p.347-354</ispartof><rights>Springer Science+Business Media, LLC 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c258y-c1a69dcda0d1429acce8bb3b703d8905d5d118f9c251f1f7df510c3d3f5e95303</citedby><cites>FETCH-LOGICAL-c258y-c1a69dcda0d1429acce8bb3b703d8905d5d118f9c251f1f7df510c3d3f5e95303</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21116712$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ma, May-Thu</creatorcontrib><creatorcontrib>Yeo, Jin-Fei</creatorcontrib><creatorcontrib>Farooqui, Akhlaq A.</creatorcontrib><creatorcontrib>Ong, Wei-Yi</creatorcontrib><title>Role of Calcium Independent Phospholipase A2 in Maintaining Mitochondrial Membrane Potential and Preventing Excessive Exocytosis in PC12 Cells</title><title>Neurochemical research</title><addtitle>Neurochem Res</addtitle><addtitle>Neurochem Res</addtitle><description>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.</description><subject>Animals</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Exocytosis - physiology</subject><subject>Isoenzymes - genetics</subject><subject>Isoenzymes - metabolism</subject><subject>Membrane Potential, Mitochondrial - physiology</subject><subject>Membrane Potentials - physiology</subject><subject>Mitochondria - metabolism</subject><subject>Naphthalenes - metabolism</subject><subject>Neurochemistry</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Original Paper</subject><subject>PC12 Cells</subject><subject>Phosphodiesterase Inhibitors - metabolism</subject><subject>Phospholipases A2, Calcium-Independent - antagonists & inhibitors</subject><subject>Phospholipases A2, Calcium-Independent - genetics</subject><subject>Phospholipases A2, Calcium-Independent - metabolism</subject><subject>Pyrones - metabolism</subject><subject>Rats</subject><issn>0364-3190</issn><issn>1573-6903</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNp9kc9u3CAQxlGVqtmmfYBcIm45OZ0xi_8cIytpImXVVdWeEQacJbLBATuKX6LPXKxNc-wBGJjffBrmI-Qc4QoBym8REYptBggZsC1kyweyQV6yrKiBnZANsJRlWMMp-RzjEyQQcvxETnNELErMN-TPT98b6jvayF7ZeaD3TpvRpM1NdH_wcTz43o4yGnqdU-voTlo3pWXdI93ZyauDdzpY2dOdGdognaF7P6Xq9Uk6TffBvKzXxN-8KhOjfTEp8mqZfLRx1dw3mNPG9H38Qj52so_m69t5Rn7f3vxq7rKHH9_vm-uHTOW8WjKFsqi10hI0bvNaKmWqtmVtCUxXNXDNNWLV1YnGDrtSdxxBMc06bmrOgJ2Ry6PuGPzzbOIkBhtV6iD17-coqi0vC45FnUg8kir4GIPpxBjsIMMiEMTqgji6INJwxeqCWFLNxZv63A5Gv1f8G3sC8iMQU8o9miCe_Bxc-vF_VP8C9W6U3Q</recordid><startdate>201102</startdate><enddate>201102</enddate><creator>Ma, May-Thu</creator><creator>Yeo, Jin-Fei</creator><creator>Farooqui, Akhlaq A.</creator><creator>Ong, Wei-Yi</creator><general>Springer US</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>201102</creationdate><title>Role of Calcium Independent Phospholipase A2 in Maintaining Mitochondrial Membrane Potential and Preventing Excessive Exocytosis in PC12 Cells</title><author>Ma, May-Thu ; Yeo, Jin-Fei ; Farooqui, Akhlaq A. ; Ong, Wei-Yi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c258y-c1a69dcda0d1429acce8bb3b703d8905d5d118f9c251f1f7df510c3d3f5e95303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Exocytosis - physiology</topic><topic>Isoenzymes - genetics</topic><topic>Isoenzymes - metabolism</topic><topic>Membrane Potential, Mitochondrial - physiology</topic><topic>Membrane Potentials - physiology</topic><topic>Mitochondria - metabolism</topic><topic>Naphthalenes - metabolism</topic><topic>Neurochemistry</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Original Paper</topic><topic>PC12 Cells</topic><topic>Phosphodiesterase Inhibitors - metabolism</topic><topic>Phospholipases A2, Calcium-Independent - antagonists & inhibitors</topic><topic>Phospholipases A2, Calcium-Independent - genetics</topic><topic>Phospholipases A2, Calcium-Independent - metabolism</topic><topic>Pyrones - metabolism</topic><topic>Rats</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ma, May-Thu</creatorcontrib><creatorcontrib>Yeo, Jin-Fei</creatorcontrib><creatorcontrib>Farooqui, Akhlaq A.</creatorcontrib><creatorcontrib>Ong, Wei-Yi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Neurochemical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ma, May-Thu</au><au>Yeo, Jin-Fei</au><au>Farooqui, Akhlaq A.</au><au>Ong, Wei-Yi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of Calcium Independent Phospholipase A2 in Maintaining Mitochondrial Membrane Potential and Preventing Excessive Exocytosis in PC12 Cells</atitle><jtitle>Neurochemical research</jtitle><stitle>Neurochem Res</stitle><addtitle>Neurochem Res</addtitle><date>2011-02</date><risdate>2011</risdate><volume>36</volume><issue>2</issue><spage>347</spage><epage>354</epage><pages>347-354</pages><issn>0364-3190</issn><eissn>1573-6903</eissn><abstract>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.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>21116712</pmid><doi>10.1007/s11064-010-0340-y</doi><tpages>8</tpages></addata></record> |
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| ispartof | Neurochemical research, 2011-02, Vol.36 (2), p.347-354 |
| issn | 0364-3190 1573-6903 |
| language | eng |
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| 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 Rats |
| title | Role of Calcium Independent Phospholipase A2 in Maintaining Mitochondrial Membrane Potential and Preventing Excessive Exocytosis in PC12 Cells |
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