Regulation of Calcium-Independent Phospholipase A2 Expression by Adrenoceptors and Sterol Regulatory Element Binding Protein—Potential Crosstalk Between Sterol and Glycerophospholipid Mediators
Calcium-independent phospholipase A 2 (iPLA 2 ) is an 85-kDa enzyme that releases docosahexaenoic acid (DHA) from glycerophospholipids. DHA can be metabolized to resolvins and neuroprotectins that have anti-inflammatory properties and effects on neural plasticity. Recent studies show an important ro...
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| Veröffentlicht in: | Molecular neurobiology 2016, Vol.53 (1), p.500-517 |
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| creator | Chew, Wee-Siong Ong, Wei-Yi |
| description | Calcium-independent phospholipase A
2
(iPLA
2
) is an 85-kDa enzyme that releases docosahexaenoic acid (DHA) from glycerophospholipids. DHA can be metabolized to resolvins and neuroprotectins that have anti-inflammatory properties and effects on neural plasticity. Recent studies show an important role of prefrontal cortical iPLA
2
in hippocampo-prefrontal cortical LTP and antidepressant-like effect of the norepinephrine reuptake inhibitor (NRI) antidepressant, maprotiline. In this study, we elucidated the cellular mechanisms through which stimulation of adrenergic receptors could lead to increased iPLA
2
expression. Treatment of SH-SY5Y neuroblastoma cells with maprotiline, another tricyclic antidepressant with noradrenaline reuptake inhibiting properties, nortriptyline, and the adrenergic receptor agonist, phenylephrine, resulted in increased iPLA
2
β mRNA expression. This increase was blocked by inhibitors to alpha-1 adrenergic receptor, mitogen-activated protein (MAP) kinase or extracellular signal-regulated kinase (ERK) 1/2, and sterol regulatory element-binding protein (SREBP). Maprotiline and phenylephrine induced binding of SREBP-2 to sterol regulatory element (SRE) region on the iPLA
2
promoter, as determined by electrophoretic mobility shift assay (EMSA). Together, results indicate that stimulation of adrenoreceptors causes increased iPLA
2
expression via MAP kinase/ERK 1/2 and SREBP, and suggest a possible mechanism for effect of CNS noradrenaline on neural plasticity and crosstalk between sterol and glycerophospholipid mediators, that may play a role in physiological or pathophysiological processes in the brain and other organs. |
| doi_str_mv | 10.1007/s12035-014-9026-9 |
| format | Article |
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2
(iPLA
2
) is an 85-kDa enzyme that releases docosahexaenoic acid (DHA) from glycerophospholipids. DHA can be metabolized to resolvins and neuroprotectins that have anti-inflammatory properties and effects on neural plasticity. Recent studies show an important role of prefrontal cortical iPLA
2
in hippocampo-prefrontal cortical LTP and antidepressant-like effect of the norepinephrine reuptake inhibitor (NRI) antidepressant, maprotiline. In this study, we elucidated the cellular mechanisms through which stimulation of adrenergic receptors could lead to increased iPLA
2
expression. Treatment of SH-SY5Y neuroblastoma cells with maprotiline, another tricyclic antidepressant with noradrenaline reuptake inhibiting properties, nortriptyline, and the adrenergic receptor agonist, phenylephrine, resulted in increased iPLA
2
β mRNA expression. This increase was blocked by inhibitors to alpha-1 adrenergic receptor, mitogen-activated protein (MAP) kinase or extracellular signal-regulated kinase (ERK) 1/2, and sterol regulatory element-binding protein (SREBP). Maprotiline and phenylephrine induced binding of SREBP-2 to sterol regulatory element (SRE) region on the iPLA
2
promoter, as determined by electrophoretic mobility shift assay (EMSA). Together, results indicate that stimulation of adrenoreceptors causes increased iPLA
2
expression via MAP kinase/ERK 1/2 and SREBP, and suggest a possible mechanism for effect of CNS noradrenaline on neural plasticity and crosstalk between sterol and glycerophospholipid mediators, that may play a role in physiological or pathophysiological processes in the brain and other organs.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-014-9026-9</identifier><identifier>PMID: 25482049</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Adrenergic Agonists - pharmacology ; Adrenergic alpha-1 Receptor Antagonists - pharmacology ; Antidepressive Agents - pharmacology ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Cell Line, Tumor ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Glycerophospholipids - physiology ; Group VI Phospholipases A2 - biosynthesis ; Humans ; MAP Kinase Signaling System - drug effects ; MAP Kinase Signaling System - physiology ; Maprotiline - pharmacology ; Neurobiology ; Neurology ; Neurosciences ; Receptor Cross-Talk - drug effects ; Receptor Cross-Talk - physiology ; Receptors, Adrenergic - physiology ; Sterol Regulatory Element Binding Protein 2 - metabolism ; Sterols - metabolism</subject><ispartof>Molecular neurobiology, 2016, Vol.53 (1), p.500-517</ispartof><rights>Springer Science+Business Media New York 2014</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3959-273a4de2d28307ad8b04ab3a554fae6d5006ddb0fa0b6d731c836b62f61870043</citedby><cites>FETCH-LOGICAL-c3959-273a4de2d28307ad8b04ab3a554fae6d5006ddb0fa0b6d731c836b62f61870043</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12035-014-9026-9$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-014-9026-9$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,781,785,27928,27929,41492,42561,51323</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25482049$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chew, Wee-Siong</creatorcontrib><creatorcontrib>Ong, Wei-Yi</creatorcontrib><title>Regulation of Calcium-Independent Phospholipase A2 Expression by Adrenoceptors and Sterol Regulatory Element Binding Protein—Potential Crosstalk Between Sterol and Glycerophospholipid Mediators</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><addtitle>Mol Neurobiol</addtitle><description>Calcium-independent phospholipase A
2
(iPLA
2
) is an 85-kDa enzyme that releases docosahexaenoic acid (DHA) from glycerophospholipids. DHA can be metabolized to resolvins and neuroprotectins that have anti-inflammatory properties and effects on neural plasticity. Recent studies show an important role of prefrontal cortical iPLA
2
in hippocampo-prefrontal cortical LTP and antidepressant-like effect of the norepinephrine reuptake inhibitor (NRI) antidepressant, maprotiline. In this study, we elucidated the cellular mechanisms through which stimulation of adrenergic receptors could lead to increased iPLA
2
expression. Treatment of SH-SY5Y neuroblastoma cells with maprotiline, another tricyclic antidepressant with noradrenaline reuptake inhibiting properties, nortriptyline, and the adrenergic receptor agonist, phenylephrine, resulted in increased iPLA
2
β mRNA expression. This increase was blocked by inhibitors to alpha-1 adrenergic receptor, mitogen-activated protein (MAP) kinase or extracellular signal-regulated kinase (ERK) 1/2, and sterol regulatory element-binding protein (SREBP). Maprotiline and phenylephrine induced binding of SREBP-2 to sterol regulatory element (SRE) region on the iPLA
2
promoter, as determined by electrophoretic mobility shift assay (EMSA). Together, results indicate that stimulation of adrenoreceptors causes increased iPLA
2
expression via MAP kinase/ERK 1/2 and SREBP, and suggest a possible mechanism for effect of CNS noradrenaline on neural plasticity and crosstalk between sterol and glycerophospholipid mediators, that may play a role in physiological or pathophysiological processes in the brain and other organs.</description><subject>Adrenergic Agonists - pharmacology</subject><subject>Adrenergic alpha-1 Receptor Antagonists - pharmacology</subject><subject>Antidepressive Agents - pharmacology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Glycerophospholipids - physiology</subject><subject>Group VI Phospholipases A2 - biosynthesis</subject><subject>Humans</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>MAP Kinase Signaling System - physiology</subject><subject>Maprotiline - pharmacology</subject><subject>Neurobiology</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Receptor Cross-Talk - drug effects</subject><subject>Receptor Cross-Talk - physiology</subject><subject>Receptors, Adrenergic - physiology</subject><subject>Sterol Regulatory Element Binding Protein 2 - metabolism</subject><subject>Sterols - metabolism</subject><issn>0893-7648</issn><issn>1559-1182</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1uFDEQhS0EIkPgAGyQl2wayu7_5WQ0JJGCGPGzttzt6omD225st2B2HCI34iacBLdmkiUbl61675OrHiGvGbxjAPX7wDjkZQasyFrgVdY-IStWlm3GWMOfkhU0bZ7VVdGckRch3AFwzqB-Ts54WTQcinZF_nzG_Wxk1M5SN9CNNL2ex-zaKpwwHTbS3a0L060zepIB6ZrT7a_JYwiLpTvQtfJoXY9TdD5QaRX9EtE7Q09k5w90a3BcUBfaKm33dOddRG3__r7fpYuNWhq68S6EKM13eoHxJ6J94CzIS3Po02N6_IpW9CMqveDDS_JskCbgq1M9J98-bL9urrKbT5fXm_VN1udtWgqvc1ko5Io3OdRSNR0UsstlWRaDxEqVAJVSHQwSukrVOeubvOoqPlSsqQGK_Jy8PXIn737MGKIYdejRGGnRzUGwulo2XjJIUnaU9stUHgcxeT1KfxAMxJKdOGYnUnZiyU60yfPmhJ-7EdWj4yGsJOBHQUgtu0cv7tzsbRr5P9R_jNGqgg</recordid><startdate>2016</startdate><enddate>2016</enddate><creator>Chew, Wee-Siong</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>2016</creationdate><title>Regulation of Calcium-Independent Phospholipase A2 Expression by Adrenoceptors and Sterol Regulatory Element Binding Protein—Potential Crosstalk Between Sterol and Glycerophospholipid Mediators</title><author>Chew, Wee-Siong ; Ong, Wei-Yi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3959-273a4de2d28307ad8b04ab3a554fae6d5006ddb0fa0b6d731c836b62f61870043</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adrenergic Agonists - pharmacology</topic><topic>Adrenergic alpha-1 Receptor Antagonists - pharmacology</topic><topic>Antidepressive Agents - pharmacology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Cell Line, Tumor</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>Glycerophospholipids - physiology</topic><topic>Group VI Phospholipases A2 - biosynthesis</topic><topic>Humans</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>MAP Kinase Signaling System - physiology</topic><topic>Maprotiline - pharmacology</topic><topic>Neurobiology</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Receptor Cross-Talk - drug effects</topic><topic>Receptor Cross-Talk - physiology</topic><topic>Receptors, Adrenergic - physiology</topic><topic>Sterol Regulatory Element Binding Protein 2 - metabolism</topic><topic>Sterols - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chew, Wee-Siong</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>Molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chew, Wee-Siong</au><au>Ong, Wei-Yi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulation of Calcium-Independent Phospholipase A2 Expression by Adrenoceptors and Sterol Regulatory Element Binding Protein—Potential Crosstalk Between Sterol and Glycerophospholipid Mediators</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><addtitle>Mol Neurobiol</addtitle><date>2016</date><risdate>2016</risdate><volume>53</volume><issue>1</issue><spage>500</spage><epage>517</epage><pages>500-517</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>Calcium-independent phospholipase A
2
(iPLA
2
) is an 85-kDa enzyme that releases docosahexaenoic acid (DHA) from glycerophospholipids. DHA can be metabolized to resolvins and neuroprotectins that have anti-inflammatory properties and effects on neural plasticity. Recent studies show an important role of prefrontal cortical iPLA
2
in hippocampo-prefrontal cortical LTP and antidepressant-like effect of the norepinephrine reuptake inhibitor (NRI) antidepressant, maprotiline. In this study, we elucidated the cellular mechanisms through which stimulation of adrenergic receptors could lead to increased iPLA
2
expression. Treatment of SH-SY5Y neuroblastoma cells with maprotiline, another tricyclic antidepressant with noradrenaline reuptake inhibiting properties, nortriptyline, and the adrenergic receptor agonist, phenylephrine, resulted in increased iPLA
2
β mRNA expression. This increase was blocked by inhibitors to alpha-1 adrenergic receptor, mitogen-activated protein (MAP) kinase or extracellular signal-regulated kinase (ERK) 1/2, and sterol regulatory element-binding protein (SREBP). Maprotiline and phenylephrine induced binding of SREBP-2 to sterol regulatory element (SRE) region on the iPLA
2
promoter, as determined by electrophoretic mobility shift assay (EMSA). Together, results indicate that stimulation of adrenoreceptors causes increased iPLA
2
expression via MAP kinase/ERK 1/2 and SREBP, and suggest a possible mechanism for effect of CNS noradrenaline on neural plasticity and crosstalk between sterol and glycerophospholipid mediators, that may play a role in physiological or pathophysiological processes in the brain and other organs.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>25482049</pmid><doi>10.1007/s12035-014-9026-9</doi><tpages>18</tpages></addata></record> |
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| subjects | Adrenergic Agonists - pharmacology Adrenergic alpha-1 Receptor Antagonists - pharmacology Antidepressive Agents - pharmacology Biomedical and Life Sciences Biomedicine Cell Biology Cell Line, Tumor Extracellular Signal-Regulated MAP Kinases - metabolism Glycerophospholipids - physiology Group VI Phospholipases A2 - biosynthesis Humans MAP Kinase Signaling System - drug effects MAP Kinase Signaling System - physiology Maprotiline - pharmacology Neurobiology Neurology Neurosciences Receptor Cross-Talk - drug effects Receptor Cross-Talk - physiology Receptors, Adrenergic - physiology Sterol Regulatory Element Binding Protein 2 - metabolism Sterols - metabolism |
| title | Regulation of Calcium-Independent Phospholipase A2 Expression by Adrenoceptors and Sterol Regulatory Element Binding Protein—Potential Crosstalk Between Sterol and Glycerophospholipid Mediators |
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