(‐)Epicatechin stimulates ERK‐dependent cyclic AMP response element activity and up‐regulates GluR2 in cortical neurons
Emerging evidence suggests that the cellular actions of flavonoids relate not simply to their antioxidant potential but also to the modulation of protein kinase signalling pathways. We investigated in primary cortical neurons, the ability of the flavan‐3‐ol, (‐)epicatechin, and its human metabolites...
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| Veröffentlicht in: | Journal of neurochemistry 2007-06, Vol.101 (6), p.1596-1606 |
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| creator | Schroeter, Hagen Bahia, Parmvir Spencer, Jeremy P. E. Sheppard, Olivia Rattray, Marcus Cadenas, Enrique Rice‐Evans, Catherine Williams, Robert J. |
| description | Emerging evidence suggests that the cellular actions of flavonoids relate not simply to their antioxidant potential but also to the modulation of protein kinase signalling pathways. We investigated in primary cortical neurons, the ability of the flavan‐3‐ol, (‐)epicatechin, and its human metabolites at physiologically relevant concentrations, to stimulate phosphorylation of the transcription factor cAMP‐response element binding protein (CREB), a regulator of neuronal viability and synaptic plasticity. (‐)Epicatechin at 100–300 nmol/L stimulated a rapid, extracellular signal‐regulated kinase (ERK)‐ and PI3K‐dependent, increase in CREB phosphorylation. At micromolar concentrations, stimulation was no longer apparent and at the highest concentration tested (30 μmol/L) (‐)epicatechin was inhibitory. (‐)Epicatechin also stimulated ERK and Akt phosphorylation with similar bell‐shaped concentration‐response characteristics. The human metabolite 3′‐O‐methyl‐(‐)epicatechin was as effective as (‐)epicatechin at stimulating ERK phosphorylation, but (‐)epicatechin glucuronide was inactive. (‐)Epicatechin and 3′‐O‐methyl‐(‐)epicatechin treatments (100 nmol/L) increased CRE‐luciferase activity in cortical neurons in a partially ERK‐dependent manner, suggesting the potential to increase CREB‐mediated gene expression. mRNA levels of the glutamate receptor subunit GluR2 increased by 60%, measured 18 h after a 15 min exposure to (‐)epicatechin and this translated into an increase in GluR2 protein. Thus, (‐)epicatechin has the potential to increase CREB‐regulated gene expression and increase GluR2 levels and thus modulate neurotransmission, plasticity and synaptogenesis. |
| doi_str_mv | 10.1111/j.1471-4159.2006.04434.x |
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E. ; Sheppard, Olivia ; Rattray, Marcus ; Cadenas, Enrique ; Rice‐Evans, Catherine ; Williams, Robert J.</creator><creatorcontrib>Schroeter, Hagen ; Bahia, Parmvir ; Spencer, Jeremy P. E. ; Sheppard, Olivia ; Rattray, Marcus ; Cadenas, Enrique ; Rice‐Evans, Catherine ; Williams, Robert J.</creatorcontrib><description>Emerging evidence suggests that the cellular actions of flavonoids relate not simply to their antioxidant potential but also to the modulation of protein kinase signalling pathways. We investigated in primary cortical neurons, the ability of the flavan‐3‐ol, (‐)epicatechin, and its human metabolites at physiologically relevant concentrations, to stimulate phosphorylation of the transcription factor cAMP‐response element binding protein (CREB), a regulator of neuronal viability and synaptic plasticity. (‐)Epicatechin at 100–300 nmol/L stimulated a rapid, extracellular signal‐regulated kinase (ERK)‐ and PI3K‐dependent, increase in CREB phosphorylation. At micromolar concentrations, stimulation was no longer apparent and at the highest concentration tested (30 μmol/L) (‐)epicatechin was inhibitory. (‐)Epicatechin also stimulated ERK and Akt phosphorylation with similar bell‐shaped concentration‐response characteristics. The human metabolite 3′‐O‐methyl‐(‐)epicatechin was as effective as (‐)epicatechin at stimulating ERK phosphorylation, but (‐)epicatechin glucuronide was inactive. (‐)Epicatechin and 3′‐O‐methyl‐(‐)epicatechin treatments (100 nmol/L) increased CRE‐luciferase activity in cortical neurons in a partially ERK‐dependent manner, suggesting the potential to increase CREB‐mediated gene expression. mRNA levels of the glutamate receptor subunit GluR2 increased by 60%, measured 18 h after a 15 min exposure to (‐)epicatechin and this translated into an increase in GluR2 protein. Thus, (‐)epicatechin has the potential to increase CREB‐regulated gene expression and increase GluR2 levels and thus modulate neurotransmission, plasticity and synaptogenesis.</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1111/j.1471-4159.2006.04434.x</identifier><identifier>PMID: 17298385</identifier><identifier>CODEN: JONRA9</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adult and adolescent clinical studies ; Akt ; Animals ; antioxidants ; Biochemistry ; Biological and medical sciences ; Bipolar disorders ; Catechin - metabolism ; Catechin - pharmacology ; Cells, Cultured ; Cerebral Cortex - drug effects ; Cerebral Cortex - metabolism ; Cyclic AMP Response Element-Binding Protein - metabolism ; cyclic AMP‐response element binding protein ; Extracellular Signal-Regulated MAP Kinases - physiology ; flavonoids ; Fundamental and applied biological sciences. Psychology ; Gene expression ; Kinases ; Medical sciences ; Mice ; mitogen‐activated protein kinase ; Molecular and cellular biology ; Molecular genetics ; Mood disorders ; neurodegeneration ; Neurology ; Neurons - drug effects ; Neurons - metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt - metabolism ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Receptors, AMPA - biosynthesis ; Ribonucleic acid ; RNA ; RNA, Messenger - metabolism ; Signal transduction ; Transcription. Transcription factor. Splicing. Rna processing ; Up-Regulation</subject><ispartof>Journal of neurochemistry, 2007-06, Vol.101 (6), p.1596-1606</ispartof><rights>2007 INIST-CNRS</rights><rights>2007 The Authors Journal Compilation 2007 International Society for Neurochemistry</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5214-b6edd336d4d4419f26b6aad7b6df23a992fb0cab4f44efee840f22f0246b12bd3</citedby><cites>FETCH-LOGICAL-c5214-b6edd336d4d4419f26b6aad7b6df23a992fb0cab4f44efee840f22f0246b12bd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1471-4159.2006.04434.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1471-4159.2006.04434.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18806939$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17298385$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schroeter, Hagen</creatorcontrib><creatorcontrib>Bahia, Parmvir</creatorcontrib><creatorcontrib>Spencer, Jeremy P. E.</creatorcontrib><creatorcontrib>Sheppard, Olivia</creatorcontrib><creatorcontrib>Rattray, Marcus</creatorcontrib><creatorcontrib>Cadenas, Enrique</creatorcontrib><creatorcontrib>Rice‐Evans, Catherine</creatorcontrib><creatorcontrib>Williams, Robert J.</creatorcontrib><title>(‐)Epicatechin stimulates ERK‐dependent cyclic AMP response element activity and up‐regulates GluR2 in cortical neurons</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>Emerging evidence suggests that the cellular actions of flavonoids relate not simply to their antioxidant potential but also to the modulation of protein kinase signalling pathways. We investigated in primary cortical neurons, the ability of the flavan‐3‐ol, (‐)epicatechin, and its human metabolites at physiologically relevant concentrations, to stimulate phosphorylation of the transcription factor cAMP‐response element binding protein (CREB), a regulator of neuronal viability and synaptic plasticity. (‐)Epicatechin at 100–300 nmol/L stimulated a rapid, extracellular signal‐regulated kinase (ERK)‐ and PI3K‐dependent, increase in CREB phosphorylation. At micromolar concentrations, stimulation was no longer apparent and at the highest concentration tested (30 μmol/L) (‐)epicatechin was inhibitory. (‐)Epicatechin also stimulated ERK and Akt phosphorylation with similar bell‐shaped concentration‐response characteristics. The human metabolite 3′‐O‐methyl‐(‐)epicatechin was as effective as (‐)epicatechin at stimulating ERK phosphorylation, but (‐)epicatechin glucuronide was inactive. (‐)Epicatechin and 3′‐O‐methyl‐(‐)epicatechin treatments (100 nmol/L) increased CRE‐luciferase activity in cortical neurons in a partially ERK‐dependent manner, suggesting the potential to increase CREB‐mediated gene expression. mRNA levels of the glutamate receptor subunit GluR2 increased by 60%, measured 18 h after a 15 min exposure to (‐)epicatechin and this translated into an increase in GluR2 protein. Thus, (‐)epicatechin has the potential to increase CREB‐regulated gene expression and increase GluR2 levels and thus modulate neurotransmission, plasticity and synaptogenesis.</description><subject>Adult and adolescent clinical studies</subject><subject>Akt</subject><subject>Animals</subject><subject>antioxidants</subject><subject>Biochemistry</subject><subject>Biological and medical sciences</subject><subject>Bipolar disorders</subject><subject>Catechin - metabolism</subject><subject>Catechin - pharmacology</subject><subject>Cells, Cultured</subject><subject>Cerebral Cortex - drug effects</subject><subject>Cerebral Cortex - metabolism</subject><subject>Cyclic AMP Response Element-Binding Protein - metabolism</subject><subject>cyclic AMP‐response element binding protein</subject><subject>Extracellular Signal-Regulated MAP Kinases - physiology</subject><subject>flavonoids</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene expression</subject><subject>Kinases</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>mitogen‐activated protein kinase</subject><subject>Molecular and cellular biology</subject><subject>Molecular genetics</subject><subject>Mood disorders</subject><subject>neurodegeneration</subject><subject>Neurology</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Phosphorylation</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>Receptors, AMPA - biosynthesis</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA, Messenger - metabolism</subject><subject>Signal transduction</subject><subject>Transcription. Transcription factor. Splicing. Rna processing</subject><subject>Up-Regulation</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkctu1DAYhS0EokPhFZCFRAWLBN_iSRYsqtHQAuWiCtaWY_8Gj3LDTkpngdRH4Bl5EhwmohIrvLGt853jXz4IYUpymtaLXU7FmmaCFlXOCJE5EYKL_PoOWv0V7qIVIYxlnAh2hB7EuCOESiHpfXRE16wqeVms0I9nv25-Pt8O3ugRzFff4Tj6dmrSLeLt5dukWhigs9CN2OxN4w0-ffcRB4hD30XA0EA7a9qM_sqPe6w7i6ch-QJ8WXLOmumS4ZRt-jCmlxrcwRSS_SG653QT4dGyH6PPr7afNufZxYez15vTi8wUjIqslmAt59IKKwStHJO11Nqua2kd47qqmKuJ0bVwQoADKAVxjDnChKwpqy0_RieH3CH03yaIo2p9NNA0uoN-iooRwRkvRAKf_APu-il0abbEyEKsK8ITVB4gE_oYAzg1BN_qsFeUqLkftVNzDWquQc39qD_9qOtkfbzkT3UL9ta4FJKApwugY_ooF3RnfLzlypLIileJe3ngvvsG9v89gHrzfjOf-G_mNq-B</recordid><startdate>200706</startdate><enddate>200706</enddate><creator>Schroeter, Hagen</creator><creator>Bahia, Parmvir</creator><creator>Spencer, Jeremy P. E.</creator><creator>Sheppard, Olivia</creator><creator>Rattray, Marcus</creator><creator>Cadenas, Enrique</creator><creator>Rice‐Evans, Catherine</creator><creator>Williams, Robert J.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><scope>IQODW</scope><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>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope></search><sort><creationdate>200706</creationdate><title>(‐)Epicatechin stimulates ERK‐dependent cyclic AMP response element activity and up‐regulates GluR2 in cortical neurons</title><author>Schroeter, Hagen ; Bahia, Parmvir ; Spencer, Jeremy P. 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Psychology</topic><topic>Gene expression</topic><topic>Kinases</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>mitogen‐activated protein kinase</topic><topic>Molecular and cellular biology</topic><topic>Molecular genetics</topic><topic>Mood disorders</topic><topic>neurodegeneration</topic><topic>Neurology</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Phosphorylation</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>Receptors, AMPA - biosynthesis</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal transduction</topic><topic>Transcription. Transcription factor. Splicing. Rna processing</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schroeter, Hagen</creatorcontrib><creatorcontrib>Bahia, Parmvir</creatorcontrib><creatorcontrib>Spencer, Jeremy P. 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E.</au><au>Sheppard, Olivia</au><au>Rattray, Marcus</au><au>Cadenas, Enrique</au><au>Rice‐Evans, Catherine</au><au>Williams, Robert J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>(‐)Epicatechin stimulates ERK‐dependent cyclic AMP response element activity and up‐regulates GluR2 in cortical neurons</atitle><jtitle>Journal of neurochemistry</jtitle><addtitle>J Neurochem</addtitle><date>2007-06</date><risdate>2007</risdate><volume>101</volume><issue>6</issue><spage>1596</spage><epage>1606</epage><pages>1596-1606</pages><issn>0022-3042</issn><eissn>1471-4159</eissn><coden>JONRA9</coden><abstract>Emerging evidence suggests that the cellular actions of flavonoids relate not simply to their antioxidant potential but also to the modulation of protein kinase signalling pathways. We investigated in primary cortical neurons, the ability of the flavan‐3‐ol, (‐)epicatechin, and its human metabolites at physiologically relevant concentrations, to stimulate phosphorylation of the transcription factor cAMP‐response element binding protein (CREB), a regulator of neuronal viability and synaptic plasticity. (‐)Epicatechin at 100–300 nmol/L stimulated a rapid, extracellular signal‐regulated kinase (ERK)‐ and PI3K‐dependent, increase in CREB phosphorylation. At micromolar concentrations, stimulation was no longer apparent and at the highest concentration tested (30 μmol/L) (‐)epicatechin was inhibitory. (‐)Epicatechin also stimulated ERK and Akt phosphorylation with similar bell‐shaped concentration‐response characteristics. The human metabolite 3′‐O‐methyl‐(‐)epicatechin was as effective as (‐)epicatechin at stimulating ERK phosphorylation, but (‐)epicatechin glucuronide was inactive. (‐)Epicatechin and 3′‐O‐methyl‐(‐)epicatechin treatments (100 nmol/L) increased CRE‐luciferase activity in cortical neurons in a partially ERK‐dependent manner, suggesting the potential to increase CREB‐mediated gene expression. mRNA levels of the glutamate receptor subunit GluR2 increased by 60%, measured 18 h after a 15 min exposure to (‐)epicatechin and this translated into an increase in GluR2 protein. Thus, (‐)epicatechin has the potential to increase CREB‐regulated gene expression and increase GluR2 levels and thus modulate neurotransmission, plasticity and synaptogenesis.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>17298385</pmid><doi>10.1111/j.1471-4159.2006.04434.x</doi><tpages>11</tpages></addata></record> |
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| subjects | Adult and adolescent clinical studies Akt Animals antioxidants Biochemistry Biological and medical sciences Bipolar disorders Catechin - metabolism Catechin - pharmacology Cells, Cultured Cerebral Cortex - drug effects Cerebral Cortex - metabolism Cyclic AMP Response Element-Binding Protein - metabolism cyclic AMP‐response element binding protein Extracellular Signal-Regulated MAP Kinases - physiology flavonoids Fundamental and applied biological sciences. Psychology Gene expression Kinases Medical sciences Mice mitogen‐activated protein kinase Molecular and cellular biology Molecular genetics Mood disorders neurodegeneration Neurology Neurons - drug effects Neurons - metabolism Phosphorylation Proto-Oncogene Proteins c-akt - metabolism Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Receptors, AMPA - biosynthesis Ribonucleic acid RNA RNA, Messenger - metabolism Signal transduction Transcription. Transcription factor. Splicing. Rna processing Up-Regulation |
| title | (‐)Epicatechin stimulates ERK‐dependent cyclic AMP response element activity and up‐regulates GluR2 in cortical neurons |
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