Localization of neuroglobin in the brain of R6/2 mouse model of Huntington’s disease
Neuroglobin (Ngb) is expressed in the central and peripheral nervous system, cerebrospinal fluid, retina, and endocrine tissues where it is involved in binding O 2 and other gasotransmitters. Several studies have highlighted its endogenous neuroprotective function. Huntington’s disease (HD), a domin...
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| Veröffentlicht in: | Neurological sciences 2018-02, Vol.39 (2), p.275-285 |
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| creator | Cardinale, A. Fusco, F. R. Paldino, E. Giampà, C. Marino, M. Nuzzo, M. T. D’Angelo, V. Laurenti, D. Straccia, G. Fasano, D. Sarnataro, D. Squillaro, T. Paladino, S. Melone, Mariarosa A. B. |
| description | Neuroglobin (Ngb) is expressed in the central and peripheral nervous system, cerebrospinal fluid, retina, and endocrine tissues where it is involved in binding O
2
and other gasotransmitters. Several studies have highlighted its endogenous neuroprotective function. Huntington’s disease (HD), a dominant hereditary disease, is characterized by the gradual loss of neurons in discrete areas of the central nervous system. We analyzed the expression of Ngb in the brain tissue of a mouse model of HD, in order to define the role of Ngb with respect to individual cell type vulnerability in HD and to gender and age of mice. Our results showed different expressions of Ngb among neurons of a specific region and between different brain regions. We evidenced a decreased intensity of Ngb at 13 weeks of age, compared to 7 weeks of age. The double immunofluorescence and fluorescence resonance energy transfer (FRET) experiments showed that the co-localization between Ngb and huntingtin at the subcellular level was not close enough to account for a direct interaction. We also observed a different expression of Ngb in the striatum, depending on the sex and age of animals. These findings provide the first experimental evidence for an adaptive response of Ngb in HD, suggesting that Ngb may exert neuroprotective effects in HD beyond its role in reducing sensitivity to oxidative stress. |
| doi_str_mv | 10.1007/s10072-017-3168-2 |
| format | Article |
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2
and other gasotransmitters. Several studies have highlighted its endogenous neuroprotective function. Huntington’s disease (HD), a dominant hereditary disease, is characterized by the gradual loss of neurons in discrete areas of the central nervous system. We analyzed the expression of Ngb in the brain tissue of a mouse model of HD, in order to define the role of Ngb with respect to individual cell type vulnerability in HD and to gender and age of mice. Our results showed different expressions of Ngb among neurons of a specific region and between different brain regions. We evidenced a decreased intensity of Ngb at 13 weeks of age, compared to 7 weeks of age. The double immunofluorescence and fluorescence resonance energy transfer (FRET) experiments showed that the co-localization between Ngb and huntingtin at the subcellular level was not close enough to account for a direct interaction. We also observed a different expression of Ngb in the striatum, depending on the sex and age of animals. These findings provide the first experimental evidence for an adaptive response of Ngb in HD, suggesting that Ngb may exert neuroprotective effects in HD beyond its role in reducing sensitivity to oxidative stress.</description><identifier>ISSN: 1590-1874</identifier><identifier>EISSN: 1590-3478</identifier><identifier>DOI: 10.1007/s10072-017-3168-2</identifier><identifier>PMID: 29101592</identifier><language>eng</language><publisher>Milan: Springer Milan</publisher><subject>ADP-Ribosylation Factors ; Age ; Animals ; Bacterial Toxins ; Cell Line, Tumor ; Central nervous system ; Cerebrospinal fluid ; Cholinesterases - metabolism ; Corpus Striatum - metabolism ; Corpus Striatum - pathology ; Disease Models, Animal ; Female ; Fluorescence Resonance Energy Transfer ; Gene Expression Regulation - genetics ; Globins - metabolism ; Huntingtin ; Huntingtin Protein - genetics ; Huntington Disease - genetics ; Huntington Disease - pathology ; Huntington's disease ; Huntingtons disease ; Immunofluorescence ; Localization ; Male ; Medicine ; Medicine & Public Health ; Mice ; Mice, Transgenic ; Mutation - genetics ; Neostriatum ; Nerve Tissue Proteins - metabolism ; Nervous system ; Neuroglobin ; Neurology ; Neurons - metabolism ; Neuroprotection ; Neuroradiology ; Neurosciences ; Neurosurgery ; Original Article ; Oxidative stress ; Parvalbumins - metabolism ; Psychiatry ; Retina ; Sex Factors ; Time Factors</subject><ispartof>Neurological sciences, 2018-02, Vol.39 (2), p.275-285</ispartof><rights>Springer-Verlag Italia S.r.l. 2017</rights><rights>Neurological Sciences is a copyright of Springer, (2017). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-244213c9b544e12f398ae30216ec9aafb4df7f2aaf75359a3442ff25c0a93e583</citedby><cites>FETCH-LOGICAL-c372t-244213c9b544e12f398ae30216ec9aafb4df7f2aaf75359a3442ff25c0a93e583</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/s10072-017-3168-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10072-017-3168-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29101592$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cardinale, A.</creatorcontrib><creatorcontrib>Fusco, F. R.</creatorcontrib><creatorcontrib>Paldino, E.</creatorcontrib><creatorcontrib>Giampà, C.</creatorcontrib><creatorcontrib>Marino, M.</creatorcontrib><creatorcontrib>Nuzzo, M. T.</creatorcontrib><creatorcontrib>D’Angelo, V.</creatorcontrib><creatorcontrib>Laurenti, D.</creatorcontrib><creatorcontrib>Straccia, G.</creatorcontrib><creatorcontrib>Fasano, D.</creatorcontrib><creatorcontrib>Sarnataro, D.</creatorcontrib><creatorcontrib>Squillaro, T.</creatorcontrib><creatorcontrib>Paladino, S.</creatorcontrib><creatorcontrib>Melone, Mariarosa A. B.</creatorcontrib><title>Localization of neuroglobin in the brain of R6/2 mouse model of Huntington’s disease</title><title>Neurological sciences</title><addtitle>Neurol Sci</addtitle><addtitle>Neurol Sci</addtitle><description>Neuroglobin (Ngb) is expressed in the central and peripheral nervous system, cerebrospinal fluid, retina, and endocrine tissues where it is involved in binding O
2
and other gasotransmitters. Several studies have highlighted its endogenous neuroprotective function. Huntington’s disease (HD), a dominant hereditary disease, is characterized by the gradual loss of neurons in discrete areas of the central nervous system. We analyzed the expression of Ngb in the brain tissue of a mouse model of HD, in order to define the role of Ngb with respect to individual cell type vulnerability in HD and to gender and age of mice. Our results showed different expressions of Ngb among neurons of a specific region and between different brain regions. We evidenced a decreased intensity of Ngb at 13 weeks of age, compared to 7 weeks of age. The double immunofluorescence and fluorescence resonance energy transfer (FRET) experiments showed that the co-localization between Ngb and huntingtin at the subcellular level was not close enough to account for a direct interaction. We also observed a different expression of Ngb in the striatum, depending on the sex and age of animals. These findings provide the first experimental evidence for an adaptive response of Ngb in HD, suggesting that Ngb may exert neuroprotective effects in HD beyond its role in reducing sensitivity to oxidative stress.</description><subject>ADP-Ribosylation Factors</subject><subject>Age</subject><subject>Animals</subject><subject>Bacterial Toxins</subject><subject>Cell Line, Tumor</subject><subject>Central nervous system</subject><subject>Cerebrospinal fluid</subject><subject>Cholinesterases - metabolism</subject><subject>Corpus Striatum - metabolism</subject><subject>Corpus Striatum - pathology</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Fluorescence Resonance Energy Transfer</subject><subject>Gene Expression Regulation - genetics</subject><subject>Globins - metabolism</subject><subject>Huntingtin</subject><subject>Huntingtin Protein - genetics</subject><subject>Huntington Disease - genetics</subject><subject>Huntington Disease - pathology</subject><subject>Huntington's disease</subject><subject>Huntingtons disease</subject><subject>Immunofluorescence</subject><subject>Localization</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Mutation - genetics</subject><subject>Neostriatum</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Nervous system</subject><subject>Neuroglobin</subject><subject>Neurology</subject><subject>Neurons - metabolism</subject><subject>Neuroprotection</subject><subject>Neuroradiology</subject><subject>Neurosciences</subject><subject>Neurosurgery</subject><subject>Original Article</subject><subject>Oxidative stress</subject><subject>Parvalbumins - metabolism</subject><subject>Psychiatry</subject><subject>Retina</subject><subject>Sex Factors</subject><subject>Time Factors</subject><issn>1590-1874</issn><issn>1590-3478</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kM9q3DAQxkVpaP60D9BLMPSSixvNSLasYwlJE1gIhKRXIXtHWwevlEr2ITnlNfJ6fZLK2U0DgYAYDfp-82n4GPsK_Dtwro7TXLHkoEoBdVPiB7YHlealkKr5uO2hUXKX7ad0yzkHCeIT20UNPIu4x34tQmeH_sGOffBFcIWnKYbVENreF_mMv6loo-2ftav6GIt1mBLluqRhfjuf_Nj71Rj838enVCz7RDbRZ7bj7JDoy_Y-YDdnp9cn5-Xi8ufFyY9F2QmFY4lSIohOt5WUBOiEbiwJjlBTp611rVw65TB3qhKVtiLzzmHVcasFVY04YEcb37sY_kyURrPuU0fDYD3lPQ3ommtUNWBGv71Bb8MUfd7OIOeoZK1AZwo2VBdDSpGcuYv92sZ7A9zMcZtN6CaHbubQzex8uHWe2jUt_0-8pJwB3AApS35F8fXr913_AVyli8Y</recordid><startdate>20180201</startdate><enddate>20180201</enddate><creator>Cardinale, A.</creator><creator>Fusco, F. R.</creator><creator>Paldino, E.</creator><creator>Giampà, C.</creator><creator>Marino, M.</creator><creator>Nuzzo, M. T.</creator><creator>D’Angelo, V.</creator><creator>Laurenti, D.</creator><creator>Straccia, G.</creator><creator>Fasano, D.</creator><creator>Sarnataro, D.</creator><creator>Squillaro, T.</creator><creator>Paladino, S.</creator><creator>Melone, Mariarosa A. 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R. ; Paldino, E. ; Giampà, C. ; Marino, M. ; Nuzzo, M. T. ; D’Angelo, V. ; Laurenti, D. ; Straccia, G. ; Fasano, D. ; Sarnataro, D. ; Squillaro, T. ; Paladino, S. ; Melone, Mariarosa A. B.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-244213c9b544e12f398ae30216ec9aafb4df7f2aaf75359a3442ff25c0a93e583</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>ADP-Ribosylation Factors</topic><topic>Age</topic><topic>Animals</topic><topic>Bacterial Toxins</topic><topic>Cell Line, Tumor</topic><topic>Central nervous system</topic><topic>Cerebrospinal fluid</topic><topic>Cholinesterases - metabolism</topic><topic>Corpus Striatum - metabolism</topic><topic>Corpus Striatum - pathology</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Fluorescence Resonance Energy Transfer</topic><topic>Gene Expression Regulation - genetics</topic><topic>Globins - metabolism</topic><topic>Huntingtin</topic><topic>Huntingtin Protein - genetics</topic><topic>Huntington Disease - genetics</topic><topic>Huntington Disease - pathology</topic><topic>Huntington's disease</topic><topic>Huntingtons disease</topic><topic>Immunofluorescence</topic><topic>Localization</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Mutation - genetics</topic><topic>Neostriatum</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Nervous system</topic><topic>Neuroglobin</topic><topic>Neurology</topic><topic>Neurons - metabolism</topic><topic>Neuroprotection</topic><topic>Neuroradiology</topic><topic>Neurosciences</topic><topic>Neurosurgery</topic><topic>Original Article</topic><topic>Oxidative stress</topic><topic>Parvalbumins - metabolism</topic><topic>Psychiatry</topic><topic>Retina</topic><topic>Sex Factors</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cardinale, A.</creatorcontrib><creatorcontrib>Fusco, F. R.</creatorcontrib><creatorcontrib>Paldino, E.</creatorcontrib><creatorcontrib>Giampà, C.</creatorcontrib><creatorcontrib>Marino, M.</creatorcontrib><creatorcontrib>Nuzzo, M. T.</creatorcontrib><creatorcontrib>D’Angelo, V.</creatorcontrib><creatorcontrib>Laurenti, D.</creatorcontrib><creatorcontrib>Straccia, G.</creatorcontrib><creatorcontrib>Fasano, D.</creatorcontrib><creatorcontrib>Sarnataro, D.</creatorcontrib><creatorcontrib>Squillaro, T.</creatorcontrib><creatorcontrib>Paladino, S.</creatorcontrib><creatorcontrib>Melone, Mariarosa A. 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R.</au><au>Paldino, E.</au><au>Giampà, C.</au><au>Marino, M.</au><au>Nuzzo, M. T.</au><au>D’Angelo, V.</au><au>Laurenti, D.</au><au>Straccia, G.</au><au>Fasano, D.</au><au>Sarnataro, D.</au><au>Squillaro, T.</au><au>Paladino, S.</au><au>Melone, Mariarosa A. B.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Localization of neuroglobin in the brain of R6/2 mouse model of Huntington’s disease</atitle><jtitle>Neurological sciences</jtitle><stitle>Neurol Sci</stitle><addtitle>Neurol Sci</addtitle><date>2018-02-01</date><risdate>2018</risdate><volume>39</volume><issue>2</issue><spage>275</spage><epage>285</epage><pages>275-285</pages><issn>1590-1874</issn><eissn>1590-3478</eissn><abstract>Neuroglobin (Ngb) is expressed in the central and peripheral nervous system, cerebrospinal fluid, retina, and endocrine tissues where it is involved in binding O
2
and other gasotransmitters. Several studies have highlighted its endogenous neuroprotective function. Huntington’s disease (HD), a dominant hereditary disease, is characterized by the gradual loss of neurons in discrete areas of the central nervous system. We analyzed the expression of Ngb in the brain tissue of a mouse model of HD, in order to define the role of Ngb with respect to individual cell type vulnerability in HD and to gender and age of mice. Our results showed different expressions of Ngb among neurons of a specific region and between different brain regions. We evidenced a decreased intensity of Ngb at 13 weeks of age, compared to 7 weeks of age. The double immunofluorescence and fluorescence resonance energy transfer (FRET) experiments showed that the co-localization between Ngb and huntingtin at the subcellular level was not close enough to account for a direct interaction. We also observed a different expression of Ngb in the striatum, depending on the sex and age of animals. These findings provide the first experimental evidence for an adaptive response of Ngb in HD, suggesting that Ngb may exert neuroprotective effects in HD beyond its role in reducing sensitivity to oxidative stress.</abstract><cop>Milan</cop><pub>Springer Milan</pub><pmid>29101592</pmid><doi>10.1007/s10072-017-3168-2</doi><tpages>11</tpages></addata></record> |
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| subjects | ADP-Ribosylation Factors Age Animals Bacterial Toxins Cell Line, Tumor Central nervous system Cerebrospinal fluid Cholinesterases - metabolism Corpus Striatum - metabolism Corpus Striatum - pathology Disease Models, Animal Female Fluorescence Resonance Energy Transfer Gene Expression Regulation - genetics Globins - metabolism Huntingtin Huntingtin Protein - genetics Huntington Disease - genetics Huntington Disease - pathology Huntington's disease Huntingtons disease Immunofluorescence Localization Male Medicine Medicine & Public Health Mice Mice, Transgenic Mutation - genetics Neostriatum Nerve Tissue Proteins - metabolism Nervous system Neuroglobin Neurology Neurons - metabolism Neuroprotection Neuroradiology Neurosciences Neurosurgery Original Article Oxidative stress Parvalbumins - metabolism Psychiatry Retina Sex Factors Time Factors |
| title | Localization of neuroglobin in the brain of R6/2 mouse model of Huntington’s disease |
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