Cardiac Noradrenaline Turnover and Heat Shock Protein 27 Phosphorylation in Dyskinetic Monkeys
Background Autonomic dysfunction is a well‐known dominant symptom in the advanced stages of Parkinson's disease. However, the role of cardiac sympathetic nerves still needs to be elucidated. Objectives To evaluate cardiac sympathetic response in Parkinsonian and dyskinetic monkeys. Methods Adul...
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| Veröffentlicht in: | Movement disorders 2020-04, Vol.35 (4), p.698-703 |
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| creator | Almela, Pilar Cuenca‐Bermejo, Lorena Yuste, José E. Estrada, Cristina Pablos, Vicente Bautista‐Hernández, Víctor Fernández‐Villalba, Emiliano Laorden, María‐Luisa Herrero, María‐Trinidad |
| description | Background
Autonomic dysfunction is a well‐known dominant symptom in the advanced stages of Parkinson's disease. However, the role of cardiac sympathetic nerves still needs to be elucidated.
Objectives
To evaluate cardiac sympathetic response in Parkinsonian and dyskinetic monkeys.
Methods
Adult male monkeys were divided into 1 of the following 3 groups: controls, 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine–treated monkeys, and 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine+levodopa–treated animals. Noradrenaline, its metabolite normetanephrine, and phospho‐Heat shock proten 27 (p‐Hsp27) at serine 82 levels were analyzed in the left and right ventricles of the heart. Tyrosine hydroxylase immunohistochemistry was performed in the ventral mesencephalon.
Results
The results were the following: (1) 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine intoxication significantly increased normetanephrine levels and decreased noradrenaline turnover in the right ventricle without changes in the left ventricle; however, (2) levodopa treatment decreased noradrenaline levels and enhanced the normetanephrine/noradrenaline ratio in parallel with a very significant increase of Hsp27 activity in both ventricles.
Conclusions
Levodopa treatment could induce protective cardiac effects through the increased Hsp27 activity. © 2019 International Parkinson and Movement Disorder Society |
| doi_str_mv | 10.1002/mds.27958 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2390686749</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2390686749</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3538-d555e2aac4fc0f966a99a37ea71502af6cf8805fa1884e00c32ad8951816a5783</originalsourceid><addsrcrecordid>eNp1kE1PwkAQhjdGI4ge_ANmE08eCvvBtrtHAyomoCTg1WbcbkOhdHG3aPrvXS168zTJm2eeybwIXVLSp4SwwTbzfZYoIY9QlwpOI8lEcoy6REoRcSpFB515vyaEUkHjU9QJWcIUFV30OgKXFaDxk3WQOVNBWVQGL_eush_GYagyPDFQ48XK6g2eO1ubosIswfOV9buVdU0JdWErHNJx4zdhuy40ntlqYxp_jk5yKL25OMweerm_W44m0fT54XF0O400F1xGmRDCMAA9zDXJVRyDUsATAwkVhEEe61xKInKgUg4NIZozyKQSVNIYRCJ5D1233p2z73vj63RtwwvhZMq4IrGMk6EK1E1LaWe9dyZPd67YgmtSStLvJtPQZPrTZGCvDsb929Zkf-RvdQEYtMBnUZrmf1M6Gy9a5RdVqHzi</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2390686749</pqid></control><display><type>article</type><title>Cardiac Noradrenaline Turnover and Heat Shock Protein 27 Phosphorylation in Dyskinetic Monkeys</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Almela, Pilar ; Cuenca‐Bermejo, Lorena ; Yuste, José E. ; Estrada, Cristina ; Pablos, Vicente ; Bautista‐Hernández, Víctor ; Fernández‐Villalba, Emiliano ; Laorden, María‐Luisa ; Herrero, María‐Trinidad</creator><creatorcontrib>Almela, Pilar ; Cuenca‐Bermejo, Lorena ; Yuste, José E. ; Estrada, Cristina ; Pablos, Vicente ; Bautista‐Hernández, Víctor ; Fernández‐Villalba, Emiliano ; Laorden, María‐Luisa ; Herrero, María‐Trinidad</creatorcontrib><description>Background
Autonomic dysfunction is a well‐known dominant symptom in the advanced stages of Parkinson's disease. However, the role of cardiac sympathetic nerves still needs to be elucidated.
Objectives
To evaluate cardiac sympathetic response in Parkinsonian and dyskinetic monkeys.
Methods
Adult male monkeys were divided into 1 of the following 3 groups: controls, 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine–treated monkeys, and 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine+levodopa–treated animals. Noradrenaline, its metabolite normetanephrine, and phospho‐Heat shock proten 27 (p‐Hsp27) at serine 82 levels were analyzed in the left and right ventricles of the heart. Tyrosine hydroxylase immunohistochemistry was performed in the ventral mesencephalon.
Results
The results were the following: (1) 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine intoxication significantly increased normetanephrine levels and decreased noradrenaline turnover in the right ventricle without changes in the left ventricle; however, (2) levodopa treatment decreased noradrenaline levels and enhanced the normetanephrine/noradrenaline ratio in parallel with a very significant increase of Hsp27 activity in both ventricles.
Conclusions
Levodopa treatment could induce protective cardiac effects through the increased Hsp27 activity. © 2019 International Parkinson and Movement Disorder Society</description><identifier>ISSN: 0885-3185</identifier><identifier>EISSN: 1531-8257</identifier><identifier>DOI: 10.1002/mds.27958</identifier><identifier>PMID: 31872915</identifier><language>eng</language><publisher>Hoboken, USA: John Wiley & Sons, Inc</publisher><subject>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine ; Animals ; Basal ganglia ; Central nervous system diseases ; Dyskinesias - metabolism ; Heart diseases ; Heat shock proteins ; Hsp27 ; HSP27 Heat-Shock Proteins ; Hsp27 protein ; Hydroxylase ; Immunohistochemistry ; Intoxication ; Levodopa ; l‐dopa ; Macaca fascicularis ; Male ; Mesencephalon ; Metabolites ; Movement disorders ; NA turnover ; Neurodegenerative diseases ; Norepinephrine ; Parkinson's disease ; Phosphorylation ; Protein turnover ; Serine ; Sympathetic nerves ; Tyrosine 3-monooxygenase ; Tyrosine 3-Monooxygenase - metabolism ; Ventricle</subject><ispartof>Movement disorders, 2020-04, Vol.35 (4), p.698-703</ispartof><rights>2019 International Parkinson and Movement Disorder Society</rights><rights>2019 International Parkinson and Movement Disorder Society.</rights><rights>2020 International Parkinson and Movement Disorder Society</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3538-d555e2aac4fc0f966a99a37ea71502af6cf8805fa1884e00c32ad8951816a5783</citedby><cites>FETCH-LOGICAL-c3538-d555e2aac4fc0f966a99a37ea71502af6cf8805fa1884e00c32ad8951816a5783</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fmds.27958$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fmds.27958$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31872915$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Almela, Pilar</creatorcontrib><creatorcontrib>Cuenca‐Bermejo, Lorena</creatorcontrib><creatorcontrib>Yuste, José E.</creatorcontrib><creatorcontrib>Estrada, Cristina</creatorcontrib><creatorcontrib>Pablos, Vicente</creatorcontrib><creatorcontrib>Bautista‐Hernández, Víctor</creatorcontrib><creatorcontrib>Fernández‐Villalba, Emiliano</creatorcontrib><creatorcontrib>Laorden, María‐Luisa</creatorcontrib><creatorcontrib>Herrero, María‐Trinidad</creatorcontrib><title>Cardiac Noradrenaline Turnover and Heat Shock Protein 27 Phosphorylation in Dyskinetic Monkeys</title><title>Movement disorders</title><addtitle>Mov Disord</addtitle><description>Background
Autonomic dysfunction is a well‐known dominant symptom in the advanced stages of Parkinson's disease. However, the role of cardiac sympathetic nerves still needs to be elucidated.
Objectives
To evaluate cardiac sympathetic response in Parkinsonian and dyskinetic monkeys.
Methods
Adult male monkeys were divided into 1 of the following 3 groups: controls, 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine–treated monkeys, and 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine+levodopa–treated animals. Noradrenaline, its metabolite normetanephrine, and phospho‐Heat shock proten 27 (p‐Hsp27) at serine 82 levels were analyzed in the left and right ventricles of the heart. Tyrosine hydroxylase immunohistochemistry was performed in the ventral mesencephalon.
Results
The results were the following: (1) 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine intoxication significantly increased normetanephrine levels and decreased noradrenaline turnover in the right ventricle without changes in the left ventricle; however, (2) levodopa treatment decreased noradrenaline levels and enhanced the normetanephrine/noradrenaline ratio in parallel with a very significant increase of Hsp27 activity in both ventricles.
Conclusions
Levodopa treatment could induce protective cardiac effects through the increased Hsp27 activity. © 2019 International Parkinson and Movement Disorder Society</description><subject>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</subject><subject>Animals</subject><subject>Basal ganglia</subject><subject>Central nervous system diseases</subject><subject>Dyskinesias - metabolism</subject><subject>Heart diseases</subject><subject>Heat shock proteins</subject><subject>Hsp27</subject><subject>HSP27 Heat-Shock Proteins</subject><subject>Hsp27 protein</subject><subject>Hydroxylase</subject><subject>Immunohistochemistry</subject><subject>Intoxication</subject><subject>Levodopa</subject><subject>l‐dopa</subject><subject>Macaca fascicularis</subject><subject>Male</subject><subject>Mesencephalon</subject><subject>Metabolites</subject><subject>Movement disorders</subject><subject>NA turnover</subject><subject>Neurodegenerative diseases</subject><subject>Norepinephrine</subject><subject>Parkinson's disease</subject><subject>Phosphorylation</subject><subject>Protein turnover</subject><subject>Serine</subject><subject>Sympathetic nerves</subject><subject>Tyrosine 3-monooxygenase</subject><subject>Tyrosine 3-Monooxygenase - metabolism</subject><subject>Ventricle</subject><issn>0885-3185</issn><issn>1531-8257</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kE1PwkAQhjdGI4ge_ANmE08eCvvBtrtHAyomoCTg1WbcbkOhdHG3aPrvXS168zTJm2eeybwIXVLSp4SwwTbzfZYoIY9QlwpOI8lEcoy6REoRcSpFB515vyaEUkHjU9QJWcIUFV30OgKXFaDxk3WQOVNBWVQGL_eush_GYagyPDFQ48XK6g2eO1ubosIswfOV9buVdU0JdWErHNJx4zdhuy40ntlqYxp_jk5yKL25OMweerm_W44m0fT54XF0O400F1xGmRDCMAA9zDXJVRyDUsATAwkVhEEe61xKInKgUg4NIZozyKQSVNIYRCJ5D1233p2z73vj63RtwwvhZMq4IrGMk6EK1E1LaWe9dyZPd67YgmtSStLvJtPQZPrTZGCvDsb929Zkf-RvdQEYtMBnUZrmf1M6Gy9a5RdVqHzi</recordid><startdate>202004</startdate><enddate>202004</enddate><creator>Almela, Pilar</creator><creator>Cuenca‐Bermejo, Lorena</creator><creator>Yuste, José E.</creator><creator>Estrada, Cristina</creator><creator>Pablos, Vicente</creator><creator>Bautista‐Hernández, Víctor</creator><creator>Fernández‐Villalba, Emiliano</creator><creator>Laorden, María‐Luisa</creator><creator>Herrero, María‐Trinidad</creator><general>John Wiley & Sons, Inc</general><general>Wiley Subscription Services, Inc</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>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>202004</creationdate><title>Cardiac Noradrenaline Turnover and Heat Shock Protein 27 Phosphorylation in Dyskinetic Monkeys</title><author>Almela, Pilar ; Cuenca‐Bermejo, Lorena ; Yuste, José E. ; Estrada, Cristina ; Pablos, Vicente ; Bautista‐Hernández, Víctor ; Fernández‐Villalba, Emiliano ; Laorden, María‐Luisa ; Herrero, María‐Trinidad</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3538-d555e2aac4fc0f966a99a37ea71502af6cf8805fa1884e00c32ad8951816a5783</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</topic><topic>Animals</topic><topic>Basal ganglia</topic><topic>Central nervous system diseases</topic><topic>Dyskinesias - metabolism</topic><topic>Heart diseases</topic><topic>Heat shock proteins</topic><topic>Hsp27</topic><topic>HSP27 Heat-Shock Proteins</topic><topic>Hsp27 protein</topic><topic>Hydroxylase</topic><topic>Immunohistochemistry</topic><topic>Intoxication</topic><topic>Levodopa</topic><topic>l‐dopa</topic><topic>Macaca fascicularis</topic><topic>Male</topic><topic>Mesencephalon</topic><topic>Metabolites</topic><topic>Movement disorders</topic><topic>NA turnover</topic><topic>Neurodegenerative diseases</topic><topic>Norepinephrine</topic><topic>Parkinson's disease</topic><topic>Phosphorylation</topic><topic>Protein turnover</topic><topic>Serine</topic><topic>Sympathetic nerves</topic><topic>Tyrosine 3-monooxygenase</topic><topic>Tyrosine 3-Monooxygenase - metabolism</topic><topic>Ventricle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Almela, Pilar</creatorcontrib><creatorcontrib>Cuenca‐Bermejo, Lorena</creatorcontrib><creatorcontrib>Yuste, José E.</creatorcontrib><creatorcontrib>Estrada, Cristina</creatorcontrib><creatorcontrib>Pablos, Vicente</creatorcontrib><creatorcontrib>Bautista‐Hernández, Víctor</creatorcontrib><creatorcontrib>Fernández‐Villalba, Emiliano</creatorcontrib><creatorcontrib>Laorden, María‐Luisa</creatorcontrib><creatorcontrib>Herrero, María‐Trinidad</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Movement disorders</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Almela, Pilar</au><au>Cuenca‐Bermejo, Lorena</au><au>Yuste, José E.</au><au>Estrada, Cristina</au><au>Pablos, Vicente</au><au>Bautista‐Hernández, Víctor</au><au>Fernández‐Villalba, Emiliano</au><au>Laorden, María‐Luisa</au><au>Herrero, María‐Trinidad</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cardiac Noradrenaline Turnover and Heat Shock Protein 27 Phosphorylation in Dyskinetic Monkeys</atitle><jtitle>Movement disorders</jtitle><addtitle>Mov Disord</addtitle><date>2020-04</date><risdate>2020</risdate><volume>35</volume><issue>4</issue><spage>698</spage><epage>703</epage><pages>698-703</pages><issn>0885-3185</issn><eissn>1531-8257</eissn><abstract>Background
Autonomic dysfunction is a well‐known dominant symptom in the advanced stages of Parkinson's disease. However, the role of cardiac sympathetic nerves still needs to be elucidated.
Objectives
To evaluate cardiac sympathetic response in Parkinsonian and dyskinetic monkeys.
Methods
Adult male monkeys were divided into 1 of the following 3 groups: controls, 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine–treated monkeys, and 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine+levodopa–treated animals. Noradrenaline, its metabolite normetanephrine, and phospho‐Heat shock proten 27 (p‐Hsp27) at serine 82 levels were analyzed in the left and right ventricles of the heart. Tyrosine hydroxylase immunohistochemistry was performed in the ventral mesencephalon.
Results
The results were the following: (1) 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine intoxication significantly increased normetanephrine levels and decreased noradrenaline turnover in the right ventricle without changes in the left ventricle; however, (2) levodopa treatment decreased noradrenaline levels and enhanced the normetanephrine/noradrenaline ratio in parallel with a very significant increase of Hsp27 activity in both ventricles.
Conclusions
Levodopa treatment could induce protective cardiac effects through the increased Hsp27 activity. © 2019 International Parkinson and Movement Disorder Society</abstract><cop>Hoboken, USA</cop><pub>John Wiley & Sons, Inc</pub><pmid>31872915</pmid><doi>10.1002/mds.27958</doi><tpages>6</tpages></addata></record> |
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| subjects | 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine Animals Basal ganglia Central nervous system diseases Dyskinesias - metabolism Heart diseases Heat shock proteins Hsp27 HSP27 Heat-Shock Proteins Hsp27 protein Hydroxylase Immunohistochemistry Intoxication Levodopa l‐dopa Macaca fascicularis Male Mesencephalon Metabolites Movement disorders NA turnover Neurodegenerative diseases Norepinephrine Parkinson's disease Phosphorylation Protein turnover Serine Sympathetic nerves Tyrosine 3-monooxygenase Tyrosine 3-Monooxygenase - metabolism Ventricle |
| title | Cardiac Noradrenaline Turnover and Heat Shock Protein 27 Phosphorylation in Dyskinetic Monkeys |
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