Histone Deacetylases Contribute to Excitotoxicity-Triggered Degeneration of Retinal Ganglion Cells In Vivo
Excitotoxicity is known to modulate the nuclear accumulation, and thus activity state, of histone deacetylases (HDACs) in pyramidal neurons. In the retina, deregulation in activity and expression of different HDACs has been linked to pathological conditions such as retinitis pigmentosa, retinal isch...
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| Veröffentlicht in: | Molecular neurobiology 2019-12, Vol.56 (12), p.8018-8034 |
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| creator | Schlüter, Annabelle Aksan, Bahar Fioravanti, Rossella Valente, Sergio Mai, Antonello Mauceri, Daniela |
| description | Excitotoxicity is known to modulate the nuclear accumulation, and thus activity state, of histone deacetylases (HDACs) in pyramidal neurons. In the retina, deregulation in activity and expression of different HDACs has been linked to pathological conditions such as retinitis pigmentosa, retinal ischemia, glaucoma, and acute optic nerve injury. Up to now, however, the effects of in vivo excitotoxicity on the different HDACs in retinal ganglion cells (RGCs) have not been thoroughly investigated. Here, we injected adult mice intravitreally with N-methyl-D-aspartate (NMDA) as a mean to trigger excitotoxicity-mediated RGC degeneration and we detected time-dependent loss of RGCs at 1 and 7 days after the insult. Further, we characterized the subcellular localization of HDACs belonging to class I (HDAC1, HDAC3), IIa (HDAC4, HDAC5, HDAC7, HDAC9), IIb (HDAC6, HDAC10), and IV (HDAC11) in RGCs. Our analyses revealed a differential pattern of HDACs nuclear distribution in RGCs following excitotoxicity. After 1 day, HDAC3, HDAC5, HDAC6, HDAC7, and HDAC11 showed altered subcellular localization in RGCs while 7 days after the excitotoxic insult, HDAC4 and HDAC9 were the only HDACs displaying changes in their subcellular distribution. Moreover, we found that in vivo selective inhibition of HDAC1/3 or HDAC4/5 via MS-275 (entinostat) or LMK-235, respectively, could prevent ongoing RGC degeneration. In conclusion, our results point towards a role of HDACs in RGC degeneration and identify HDAC1/3 and HDAC4/5 as potential therapeutic targets to treat degenerative retinal diseases. |
| doi_str_mv | 10.1007/s12035-019-01658-x |
| format | Article |
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In the retina, deregulation in activity and expression of different HDACs has been linked to pathological conditions such as retinitis pigmentosa, retinal ischemia, glaucoma, and acute optic nerve injury. Up to now, however, the effects of in vivo excitotoxicity on the different HDACs in retinal ganglion cells (RGCs) have not been thoroughly investigated. Here, we injected adult mice intravitreally with N-methyl-D-aspartate (NMDA) as a mean to trigger excitotoxicity-mediated RGC degeneration and we detected time-dependent loss of RGCs at 1 and 7 days after the insult. Further, we characterized the subcellular localization of HDACs belonging to class I (HDAC1, HDAC3), IIa (HDAC4, HDAC5, HDAC7, HDAC9), IIb (HDAC6, HDAC10), and IV (HDAC11) in RGCs. Our analyses revealed a differential pattern of HDACs nuclear distribution in RGCs following excitotoxicity. After 1 day, HDAC3, HDAC5, HDAC6, HDAC7, and HDAC11 showed altered subcellular localization in RGCs while 7 days after the excitotoxic insult, HDAC4 and HDAC9 were the only HDACs displaying changes in their subcellular distribution. Moreover, we found that in vivo selective inhibition of HDAC1/3 or HDAC4/5 via MS-275 (entinostat) or LMK-235, respectively, could prevent ongoing RGC degeneration. In conclusion, our results point towards a role of HDACs in RGC degeneration and identify HDAC1/3 and HDAC4/5 as potential therapeutic targets to treat degenerative retinal diseases.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-019-01658-x</identifier><identifier>PMID: 31161423</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Degeneration ; Deregulation ; Excitatory Amino Acid Agonists - toxicity ; Excitotoxicity ; Female ; Glaucoma ; Glutamic acid receptors ; Histone Deacetylase Inhibitors - administration & dosage ; Histone Deacetylases - metabolism ; Intravitreal Injections - methods ; Ischemia ; Localization ; Male ; Mice ; Mice, Inbred C57BL ; N-Methyl-D-aspartic acid ; N-Methylaspartate - toxicity ; Neurobiology ; Neurology ; Neurosciences ; Optic nerve ; Pyramidal cells ; Retina ; Retinal Degeneration - chemically induced ; Retinal Degeneration - drug therapy ; Retinal Degeneration - enzymology ; Retinal ganglion cells ; Retinal Ganglion Cells - drug effects ; Retinal Ganglion Cells - enzymology ; Retinitis ; Retinitis pigmentosa ; Therapeutic applications</subject><ispartof>Molecular neurobiology, 2019-12, Vol.56 (12), p.8018-8034</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2019</rights><rights>Molecular Neurobiology is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-379e170a97158b0833262b9fd3b76fe9438867ec0034afd78be3389fdb84251e3</citedby><cites>FETCH-LOGICAL-c375t-379e170a97158b0833262b9fd3b76fe9438867ec0034afd78be3389fdb84251e3</cites><orcidid>0000-0003-1225-4633</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12035-019-01658-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-019-01658-x$$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/31161423$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schlüter, Annabelle</creatorcontrib><creatorcontrib>Aksan, Bahar</creatorcontrib><creatorcontrib>Fioravanti, Rossella</creatorcontrib><creatorcontrib>Valente, Sergio</creatorcontrib><creatorcontrib>Mai, Antonello</creatorcontrib><creatorcontrib>Mauceri, Daniela</creatorcontrib><title>Histone Deacetylases Contribute to Excitotoxicity-Triggered Degeneration of Retinal Ganglion Cells In Vivo</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><addtitle>Mol Neurobiol</addtitle><description>Excitotoxicity is known to modulate the nuclear accumulation, and thus activity state, of histone deacetylases (HDACs) in pyramidal neurons. In the retina, deregulation in activity and expression of different HDACs has been linked to pathological conditions such as retinitis pigmentosa, retinal ischemia, glaucoma, and acute optic nerve injury. Up to now, however, the effects of in vivo excitotoxicity on the different HDACs in retinal ganglion cells (RGCs) have not been thoroughly investigated. Here, we injected adult mice intravitreally with N-methyl-D-aspartate (NMDA) as a mean to trigger excitotoxicity-mediated RGC degeneration and we detected time-dependent loss of RGCs at 1 and 7 days after the insult. Further, we characterized the subcellular localization of HDACs belonging to class I (HDAC1, HDAC3), IIa (HDAC4, HDAC5, HDAC7, HDAC9), IIb (HDAC6, HDAC10), and IV (HDAC11) in RGCs. Our analyses revealed a differential pattern of HDACs nuclear distribution in RGCs following excitotoxicity. After 1 day, HDAC3, HDAC5, HDAC6, HDAC7, and HDAC11 showed altered subcellular localization in RGCs while 7 days after the excitotoxic insult, HDAC4 and HDAC9 were the only HDACs displaying changes in their subcellular distribution. Moreover, we found that in vivo selective inhibition of HDAC1/3 or HDAC4/5 via MS-275 (entinostat) or LMK-235, respectively, could prevent ongoing RGC degeneration. In conclusion, our results point towards a role of HDACs in RGC degeneration and identify HDAC1/3 and HDAC4/5 as potential therapeutic targets to treat degenerative retinal diseases.</description><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Degeneration</subject><subject>Deregulation</subject><subject>Excitatory Amino Acid Agonists - toxicity</subject><subject>Excitotoxicity</subject><subject>Female</subject><subject>Glaucoma</subject><subject>Glutamic acid receptors</subject><subject>Histone Deacetylase Inhibitors - administration & dosage</subject><subject>Histone Deacetylases - metabolism</subject><subject>Intravitreal Injections - methods</subject><subject>Ischemia</subject><subject>Localization</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>N-Methyl-D-aspartic acid</subject><subject>N-Methylaspartate - toxicity</subject><subject>Neurobiology</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Optic nerve</subject><subject>Pyramidal cells</subject><subject>Retina</subject><subject>Retinal Degeneration - chemically induced</subject><subject>Retinal Degeneration - drug therapy</subject><subject>Retinal Degeneration - enzymology</subject><subject>Retinal ganglion cells</subject><subject>Retinal Ganglion Cells - drug effects</subject><subject>Retinal Ganglion Cells - enzymology</subject><subject>Retinitis</subject><subject>Retinitis pigmentosa</subject><subject>Therapeutic applications</subject><issn>0893-7648</issn><issn>1559-1182</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kE1LAzEQhoMotn78AQ8S8LyaSXY32aPUqoWCINVryG5nS8q6qUkq7b83tX7cPAwDM-_7zvAQcgHsGhiTNwE4E0XGoEpVFirbHJAhFEWVASh-SIZMVSKTZa4G5CSEJWOcA5PHZCAASsi5GJLlow3R9Ujv0DQYt50JGOjI9dHbeh2RRkfHm8ZGF93Gpr7NZt4uFuhxnjwL7NGbaF1PXUufMdredPTB9ItuNxth1wU66emr_XBn5Kg1XcDz735KXu7Hs9FjNn16mIxup1kjZBEzISsEyUwloVA1U0LwktdVOxe1LFuscqFUKbFhTOSmnUtVoxAq7WuV8wJQnJKrfe7Ku_c1hqiXbu3TX0FzLnKuJFSQVHyvarwLwWOrV96-Gb_VwPQOr97j1Qmv_sKrN8l0-R29rt9w_mv54ZkEYi8IadUnSn-3_4n9BCyShmE</recordid><startdate>20191201</startdate><enddate>20191201</enddate><creator>Schlüter, Annabelle</creator><creator>Aksan, Bahar</creator><creator>Fioravanti, Rossella</creator><creator>Valente, Sergio</creator><creator>Mai, Antonello</creator><creator>Mauceri, Daniela</creator><general>Springer US</general><general>Springer Nature B.V</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>3V.</scope><scope>7QR</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><orcidid>https://orcid.org/0000-0003-1225-4633</orcidid></search><sort><creationdate>20191201</creationdate><title>Histone Deacetylases Contribute to Excitotoxicity-Triggered Degeneration of Retinal Ganglion Cells In Vivo</title><author>Schlüter, Annabelle ; Aksan, Bahar ; Fioravanti, Rossella ; Valente, Sergio ; Mai, Antonello ; Mauceri, Daniela</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-379e170a97158b0833262b9fd3b76fe9438867ec0034afd78be3389fdb84251e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Degeneration</topic><topic>Deregulation</topic><topic>Excitatory Amino Acid Agonists - toxicity</topic><topic>Excitotoxicity</topic><topic>Female</topic><topic>Glaucoma</topic><topic>Glutamic acid receptors</topic><topic>Histone Deacetylase Inhibitors - administration & dosage</topic><topic>Histone Deacetylases - metabolism</topic><topic>Intravitreal Injections - methods</topic><topic>Ischemia</topic><topic>Localization</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>N-Methyl-D-aspartic acid</topic><topic>N-Methylaspartate - toxicity</topic><topic>Neurobiology</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Optic nerve</topic><topic>Pyramidal cells</topic><topic>Retina</topic><topic>Retinal Degeneration - chemically induced</topic><topic>Retinal Degeneration - drug therapy</topic><topic>Retinal Degeneration - enzymology</topic><topic>Retinal ganglion cells</topic><topic>Retinal Ganglion Cells - drug effects</topic><topic>Retinal Ganglion Cells - enzymology</topic><topic>Retinitis</topic><topic>Retinitis pigmentosa</topic><topic>Therapeutic applications</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schlüter, Annabelle</creatorcontrib><creatorcontrib>Aksan, Bahar</creatorcontrib><creatorcontrib>Fioravanti, Rossella</creatorcontrib><creatorcontrib>Valente, Sergio</creatorcontrib><creatorcontrib>Mai, Antonello</creatorcontrib><creatorcontrib>Mauceri, Daniela</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><jtitle>Molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schlüter, Annabelle</au><au>Aksan, Bahar</au><au>Fioravanti, Rossella</au><au>Valente, Sergio</au><au>Mai, Antonello</au><au>Mauceri, Daniela</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Histone Deacetylases Contribute to Excitotoxicity-Triggered Degeneration of Retinal Ganglion Cells In Vivo</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><addtitle>Mol Neurobiol</addtitle><date>2019-12-01</date><risdate>2019</risdate><volume>56</volume><issue>12</issue><spage>8018</spage><epage>8034</epage><pages>8018-8034</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>Excitotoxicity is known to modulate the nuclear accumulation, and thus activity state, of histone deacetylases (HDACs) in pyramidal neurons. In the retina, deregulation in activity and expression of different HDACs has been linked to pathological conditions such as retinitis pigmentosa, retinal ischemia, glaucoma, and acute optic nerve injury. Up to now, however, the effects of in vivo excitotoxicity on the different HDACs in retinal ganglion cells (RGCs) have not been thoroughly investigated. Here, we injected adult mice intravitreally with N-methyl-D-aspartate (NMDA) as a mean to trigger excitotoxicity-mediated RGC degeneration and we detected time-dependent loss of RGCs at 1 and 7 days after the insult. Further, we characterized the subcellular localization of HDACs belonging to class I (HDAC1, HDAC3), IIa (HDAC4, HDAC5, HDAC7, HDAC9), IIb (HDAC6, HDAC10), and IV (HDAC11) in RGCs. Our analyses revealed a differential pattern of HDACs nuclear distribution in RGCs following excitotoxicity. After 1 day, HDAC3, HDAC5, HDAC6, HDAC7, and HDAC11 showed altered subcellular localization in RGCs while 7 days after the excitotoxic insult, HDAC4 and HDAC9 were the only HDACs displaying changes in their subcellular distribution. Moreover, we found that in vivo selective inhibition of HDAC1/3 or HDAC4/5 via MS-275 (entinostat) or LMK-235, respectively, could prevent ongoing RGC degeneration. In conclusion, our results point towards a role of HDACs in RGC degeneration and identify HDAC1/3 and HDAC4/5 as potential therapeutic targets to treat degenerative retinal diseases.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>31161423</pmid><doi>10.1007/s12035-019-01658-x</doi><tpages>17</tpages><orcidid>https://orcid.org/0000-0003-1225-4633</orcidid></addata></record> |
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| subjects | Animals Biomedical and Life Sciences Biomedicine Cell Biology Degeneration Deregulation Excitatory Amino Acid Agonists - toxicity Excitotoxicity Female Glaucoma Glutamic acid receptors Histone Deacetylase Inhibitors - administration & dosage Histone Deacetylases - metabolism Intravitreal Injections - methods Ischemia Localization Male Mice Mice, Inbred C57BL N-Methyl-D-aspartic acid N-Methylaspartate - toxicity Neurobiology Neurology Neurosciences Optic nerve Pyramidal cells Retina Retinal Degeneration - chemically induced Retinal Degeneration - drug therapy Retinal Degeneration - enzymology Retinal ganglion cells Retinal Ganglion Cells - drug effects Retinal Ganglion Cells - enzymology Retinitis Retinitis pigmentosa Therapeutic applications |
| title | Histone Deacetylases Contribute to Excitotoxicity-Triggered Degeneration of Retinal Ganglion Cells In Vivo |
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