S100B is increased in Parkinson's disease and ablation protects against MPTP-induced toxicity through the RAGE and TNF-α pathway
Parkinson's disease is a neurodegenerative disorder that can, at least partly, be mimicked by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. S100B is a calcium-binding protein expressed in, and secreted by, astrocytes. There is increasing evidence that S100B acts as a cytokine or...
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| Veröffentlicht in: | Brain (London, England : 1878) England : 1878), 2012-11, Vol.135 (Pt 11), p.3336-3347 |
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| creator | SATHE, Kinnari MAETZLER, Walter ITOHARA, Shigeyoshi BERG, Daniela TEISMANN, Peter LANG, Johannes D MOUNSEY, Ross B FLECKENSTEIN, Corina MARTIN, Heather L SCHULTE, Claudia MUSTAFA, Sarah SYNOFZIK, Matthis VUKOVIC, Zvonimir |
| description | Parkinson's disease is a neurodegenerative disorder that can, at least partly, be mimicked by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. S100B is a calcium-binding protein expressed in, and secreted by, astrocytes. There is increasing evidence that S100B acts as a cytokine or damage-associated molecular pattern protein not only in inflammatory but also in neurodegenerative diseases. In this study, we show that S100B protein levels were higher in post-mortem substantia nigra of patients with Parkinson's disease compared with control tissue, and cerebrospinal fluid S100B levels were higher in a large cohort of patients with Parkinson's disease compared with controls. Correspondingly, mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine showed upregulated S100B messenger RNA and protein levels. In turn, ablation of S100B resulted in neuroprotection, reduced microgliosis and reduced expression of both the receptor for advanced glycation endproducts and tumour necrosis factor-α. Our results demonstrate a role of S100B in the pathophysiology of Parkinson's disease. Targeting S100B may emerge as a potential treatment strategy in this disorder. |
| doi_str_mv | 10.1093/brain/aws250 |
| format | Article |
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S100B is a calcium-binding protein expressed in, and secreted by, astrocytes. There is increasing evidence that S100B acts as a cytokine or damage-associated molecular pattern protein not only in inflammatory but also in neurodegenerative diseases. In this study, we show that S100B protein levels were higher in post-mortem substantia nigra of patients with Parkinson's disease compared with control tissue, and cerebrospinal fluid S100B levels were higher in a large cohort of patients with Parkinson's disease compared with controls. Correspondingly, mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine showed upregulated S100B messenger RNA and protein levels. In turn, ablation of S100B resulted in neuroprotection, reduced microgliosis and reduced expression of both the receptor for advanced glycation endproducts and tumour necrosis factor-α. Our results demonstrate a role of S100B in the pathophysiology of Parkinson's disease. Targeting S100B may emerge as a potential treatment strategy in this disorder.</description><identifier>ISSN: 0006-8950</identifier><identifier>EISSN: 1460-2156</identifier><identifier>DOI: 10.1093/brain/aws250</identifier><identifier>PMID: 23169921</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine - antagonists & inhibitors ; Advanced glycosylation end products ; Aged ; Animals ; Astrocytes ; Biological and medical sciences ; Calcium-binding protein ; Case-Control Studies ; Cell Line ; Cerebrospinal fluid ; Cytokines ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Disease Models, Animal ; Female ; Gliosis - pathology ; Humans ; Inflammation ; Male ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Movement disorders ; MPTP ; mRNA ; Nerve Growth Factors - genetics ; Nerve Growth Factors - metabolism ; Neurodegenerative diseases ; Neurology ; Neuroprotection ; Neuroprotective Agents - metabolism ; Neurotoxicity ; Neurotoxins ; Original ; Parkinson Disease - blood ; Parkinson Disease - cerebrospinal fluid ; Parkinson Disease - genetics ; Parkinson Disease - metabolism ; Parkinson Disease - pathology ; Parkinson's disease ; Receptor for Advanced Glycation End Products ; Receptors, Immunologic - metabolism ; S100 beta protein ; S100 Calcium Binding Protein beta Subunit ; S100 Proteins - genetics ; S100 Proteins - metabolism ; Substantia nigra ; Substantia Nigra - metabolism ; Substantia Nigra - pathology ; Tumor necrosis factor- alpha ; Tumor Necrosis Factor-alpha - metabolism ; Up-Regulation</subject><ispartof>Brain (London, England : 1878), 2012-11, Vol.135 (Pt 11), p.3336-3347</ispartof><rights>2014 INIST-CNRS</rights><rights>The Author (2012). Published by Oxford University Press on behalf of the Guarantors of Brain. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c447t-a83de1aff15d315595d9b7a3c6763f9545872221200c323d076354e709ab09023</citedby><cites>FETCH-LOGICAL-c447t-a83de1aff15d315595d9b7a3c6763f9545872221200c323d076354e709ab09023</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26646850$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23169921$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SATHE, Kinnari</creatorcontrib><creatorcontrib>MAETZLER, Walter</creatorcontrib><creatorcontrib>ITOHARA, Shigeyoshi</creatorcontrib><creatorcontrib>BERG, Daniela</creatorcontrib><creatorcontrib>TEISMANN, Peter</creatorcontrib><creatorcontrib>LANG, Johannes D</creatorcontrib><creatorcontrib>MOUNSEY, Ross B</creatorcontrib><creatorcontrib>FLECKENSTEIN, Corina</creatorcontrib><creatorcontrib>MARTIN, Heather L</creatorcontrib><creatorcontrib>SCHULTE, Claudia</creatorcontrib><creatorcontrib>MUSTAFA, Sarah</creatorcontrib><creatorcontrib>SYNOFZIK, Matthis</creatorcontrib><creatorcontrib>VUKOVIC, Zvonimir</creatorcontrib><title>S100B is increased in Parkinson's disease and ablation protects against MPTP-induced toxicity through the RAGE and TNF-α pathway</title><title>Brain (London, England : 1878)</title><addtitle>Brain</addtitle><description>Parkinson's disease is a neurodegenerative disorder that can, at least partly, be mimicked by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. S100B is a calcium-binding protein expressed in, and secreted by, astrocytes. There is increasing evidence that S100B acts as a cytokine or damage-associated molecular pattern protein not only in inflammatory but also in neurodegenerative diseases. In this study, we show that S100B protein levels were higher in post-mortem substantia nigra of patients with Parkinson's disease compared with control tissue, and cerebrospinal fluid S100B levels were higher in a large cohort of patients with Parkinson's disease compared with controls. Correspondingly, mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine showed upregulated S100B messenger RNA and protein levels. In turn, ablation of S100B resulted in neuroprotection, reduced microgliosis and reduced expression of both the receptor for advanced glycation endproducts and tumour necrosis factor-α. Our results demonstrate a role of S100B in the pathophysiology of Parkinson's disease. Targeting S100B may emerge as a potential treatment strategy in this disorder.</description><subject>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine - antagonists & inhibitors</subject><subject>Advanced glycosylation end products</subject><subject>Aged</subject><subject>Animals</subject><subject>Astrocytes</subject><subject>Biological and medical sciences</subject><subject>Calcium-binding protein</subject><subject>Case-Control Studies</subject><subject>Cell Line</subject><subject>Cerebrospinal fluid</subject><subject>Cytokines</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Gliosis - pathology</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Movement disorders</subject><subject>MPTP</subject><subject>mRNA</subject><subject>Nerve Growth Factors - genetics</subject><subject>Nerve Growth Factors - metabolism</subject><subject>Neurodegenerative diseases</subject><subject>Neurology</subject><subject>Neuroprotection</subject><subject>Neuroprotective Agents - metabolism</subject><subject>Neurotoxicity</subject><subject>Neurotoxins</subject><subject>Original</subject><subject>Parkinson Disease - blood</subject><subject>Parkinson Disease - cerebrospinal fluid</subject><subject>Parkinson Disease - genetics</subject><subject>Parkinson Disease - metabolism</subject><subject>Parkinson Disease - pathology</subject><subject>Parkinson's disease</subject><subject>Receptor for Advanced Glycation End Products</subject><subject>Receptors, Immunologic - metabolism</subject><subject>S100 beta protein</subject><subject>S100 Calcium Binding Protein beta Subunit</subject><subject>S100 Proteins - genetics</subject><subject>S100 Proteins - metabolism</subject><subject>Substantia nigra</subject><subject>Substantia Nigra - metabolism</subject><subject>Substantia Nigra - pathology</subject><subject>Tumor necrosis factor- alpha</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Up-Regulation</subject><issn>0006-8950</issn><issn>1460-2156</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkcFuEzEQhi0EoqFw44x8QXBg6dhee-NLpVK1BalABOG8mni9iWFjB9tLyZFH4kV4JtwmFDjNaObTNyP9hDxm8JKBFkeLiM4f4VXiEu6QCasVVJxJdZdMAEBVUy3hgDxI6TMAqwVX98kBF0xpzdmE_PjIAF5Rl6jzJlpMtisdnWH84nwK_lminUvXc4q-o7gYMLvg6SaGbE1OFJflfMr07Ww-q5zvRlMMOXx3xuUtzasYxuWqVEs_nFyc3Ujm786rXz_pBvPqCrcPyb0eh2Qf7esh-XR-Nj99XV2-v3hzenJZmbpucoVT0VmGfc9kJ5iUWnZ60aAwqlGi17KW04ZzzjiAEVx0UMaytg1oXIAGLg7J8c67GRdr2xnrc8Sh3US3xrhtA7r2_413q3YZvrVCAtMNK4Lne0EMX0ebcrt2ydhhQG_DmFrGZdMIUUNT0Bc71MSQUrT97RkG7XVq7U1q7S61gj_597Vb-E9MBXi6BzAZHPqI3rj0l1OqVtMi-g2KOqJI</recordid><startdate>20121101</startdate><enddate>20121101</enddate><creator>SATHE, Kinnari</creator><creator>MAETZLER, Walter</creator><creator>ITOHARA, Shigeyoshi</creator><creator>BERG, Daniela</creator><creator>TEISMANN, Peter</creator><creator>LANG, Johannes D</creator><creator>MOUNSEY, Ross B</creator><creator>FLECKENSTEIN, Corina</creator><creator>MARTIN, Heather L</creator><creator>SCHULTE, Claudia</creator><creator>MUSTAFA, Sarah</creator><creator>SYNOFZIK, Matthis</creator><creator>VUKOVIC, Zvonimir</creator><general>Oxford University Press</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>7TK</scope><scope>5PM</scope></search><sort><creationdate>20121101</creationdate><title>S100B is increased in Parkinson's disease and ablation protects against MPTP-induced toxicity through the RAGE and TNF-α pathway</title><author>SATHE, Kinnari ; MAETZLER, Walter ; ITOHARA, Shigeyoshi ; BERG, Daniela ; TEISMANN, Peter ; LANG, Johannes D ; MOUNSEY, Ross B ; FLECKENSTEIN, Corina ; MARTIN, Heather L ; SCHULTE, Claudia ; MUSTAFA, Sarah ; SYNOFZIK, Matthis ; VUKOVIC, Zvonimir</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c447t-a83de1aff15d315595d9b7a3c6763f9545872221200c323d076354e709ab09023</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine - antagonists & inhibitors</topic><topic>Advanced glycosylation end products</topic><topic>Aged</topic><topic>Animals</topic><topic>Astrocytes</topic><topic>Biological and medical sciences</topic><topic>Calcium-binding protein</topic><topic>Case-Control Studies</topic><topic>Cell Line</topic><topic>Cerebrospinal fluid</topic><topic>Cytokines</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Gliosis - pathology</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Movement disorders</topic><topic>MPTP</topic><topic>mRNA</topic><topic>Nerve Growth Factors - genetics</topic><topic>Nerve Growth Factors - metabolism</topic><topic>Neurodegenerative diseases</topic><topic>Neurology</topic><topic>Neuroprotection</topic><topic>Neuroprotective Agents - metabolism</topic><topic>Neurotoxicity</topic><topic>Neurotoxins</topic><topic>Original</topic><topic>Parkinson Disease - blood</topic><topic>Parkinson Disease - cerebrospinal fluid</topic><topic>Parkinson Disease - genetics</topic><topic>Parkinson Disease - metabolism</topic><topic>Parkinson Disease - pathology</topic><topic>Parkinson's disease</topic><topic>Receptor for Advanced Glycation End Products</topic><topic>Receptors, Immunologic - metabolism</topic><topic>S100 beta protein</topic><topic>S100 Calcium Binding Protein beta Subunit</topic><topic>S100 Proteins - genetics</topic><topic>S100 Proteins - metabolism</topic><topic>Substantia nigra</topic><topic>Substantia Nigra - metabolism</topic><topic>Substantia Nigra - pathology</topic><topic>Tumor necrosis factor- alpha</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SATHE, Kinnari</creatorcontrib><creatorcontrib>MAETZLER, Walter</creatorcontrib><creatorcontrib>ITOHARA, Shigeyoshi</creatorcontrib><creatorcontrib>BERG, Daniela</creatorcontrib><creatorcontrib>TEISMANN, Peter</creatorcontrib><creatorcontrib>LANG, Johannes D</creatorcontrib><creatorcontrib>MOUNSEY, Ross B</creatorcontrib><creatorcontrib>FLECKENSTEIN, Corina</creatorcontrib><creatorcontrib>MARTIN, Heather L</creatorcontrib><creatorcontrib>SCHULTE, Claudia</creatorcontrib><creatorcontrib>MUSTAFA, Sarah</creatorcontrib><creatorcontrib>SYNOFZIK, Matthis</creatorcontrib><creatorcontrib>VUKOVIC, Zvonimir</creatorcontrib><collection>Pascal-Francis</collection><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>PubMed Central (Full Participant titles)</collection><jtitle>Brain (London, England : 1878)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SATHE, Kinnari</au><au>MAETZLER, Walter</au><au>ITOHARA, Shigeyoshi</au><au>BERG, Daniela</au><au>TEISMANN, Peter</au><au>LANG, Johannes D</au><au>MOUNSEY, Ross B</au><au>FLECKENSTEIN, Corina</au><au>MARTIN, Heather L</au><au>SCHULTE, Claudia</au><au>MUSTAFA, Sarah</au><au>SYNOFZIK, Matthis</au><au>VUKOVIC, Zvonimir</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>S100B is increased in Parkinson's disease and ablation protects against MPTP-induced toxicity through the RAGE and TNF-α pathway</atitle><jtitle>Brain (London, England : 1878)</jtitle><addtitle>Brain</addtitle><date>2012-11-01</date><risdate>2012</risdate><volume>135</volume><issue>Pt 11</issue><spage>3336</spage><epage>3347</epage><pages>3336-3347</pages><issn>0006-8950</issn><eissn>1460-2156</eissn><abstract>Parkinson's disease is a neurodegenerative disorder that can, at least partly, be mimicked by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. S100B is a calcium-binding protein expressed in, and secreted by, astrocytes. There is increasing evidence that S100B acts as a cytokine or damage-associated molecular pattern protein not only in inflammatory but also in neurodegenerative diseases. In this study, we show that S100B protein levels were higher in post-mortem substantia nigra of patients with Parkinson's disease compared with control tissue, and cerebrospinal fluid S100B levels were higher in a large cohort of patients with Parkinson's disease compared with controls. Correspondingly, mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine showed upregulated S100B messenger RNA and protein levels. In turn, ablation of S100B resulted in neuroprotection, reduced microgliosis and reduced expression of both the receptor for advanced glycation endproducts and tumour necrosis factor-α. Our results demonstrate a role of S100B in the pathophysiology of Parkinson's disease. Targeting S100B may emerge as a potential treatment strategy in this disorder.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>23169921</pmid><doi>10.1093/brain/aws250</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Brain (London, England : 1878), 2012-11, Vol.135 (Pt 11), p.3336-3347 |
| issn | 0006-8950 1460-2156 |
| language | eng |
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| source | MEDLINE; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine - antagonists & inhibitors Advanced glycosylation end products Aged Animals Astrocytes Biological and medical sciences Calcium-binding protein Case-Control Studies Cell Line Cerebrospinal fluid Cytokines Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Disease Models, Animal Female Gliosis - pathology Humans Inflammation Male Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Movement disorders MPTP mRNA Nerve Growth Factors - genetics Nerve Growth Factors - metabolism Neurodegenerative diseases Neurology Neuroprotection Neuroprotective Agents - metabolism Neurotoxicity Neurotoxins Original Parkinson Disease - blood Parkinson Disease - cerebrospinal fluid Parkinson Disease - genetics Parkinson Disease - metabolism Parkinson Disease - pathology Parkinson's disease Receptor for Advanced Glycation End Products Receptors, Immunologic - metabolism S100 beta protein S100 Calcium Binding Protein beta Subunit S100 Proteins - genetics S100 Proteins - metabolism Substantia nigra Substantia Nigra - metabolism Substantia Nigra - pathology Tumor necrosis factor- alpha Tumor Necrosis Factor-alpha - metabolism Up-Regulation |
| title | S100B is increased in Parkinson's disease and ablation protects against MPTP-induced toxicity through the RAGE and TNF-α pathway |
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