BDNF improves axon transportation and rescues visual function in a rodent model of acute elevation of intraocular pressure
Optic neuropathies lead to blindness; the common pathology is the degeneration of axons of the retinal ganglion cells. In this study, we used a rat model of retinal ischemia-reperfusion and a one-time intravitreal brain-derived neurotrophic factor (BDNF) injection; then we examined axon transportati...
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Veröffentlicht in: | Science China. Life sciences 2020-09, Vol.63 (9), p.1337-1346 |
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description | Optic neuropathies lead to blindness; the common pathology is the degeneration of axons of the retinal ganglion cells. In this study, we used a rat model of retinal ischemia-reperfusion and a one-time intravitreal brain-derived neurotrophic factor (BDNF) injection; then we examined axon transportation function, continuity, physical presence of axons in different part of the optic nerve, and the expression level of proteins involved in axon transportation. We found that in the disease model, axon transportation was the most severely affected, followed by axon continuity, then the number of axons in the distal and proximal optic nerve. BDNF treatment relieved all reductions and significantly restored function. The molecular changes were more minor, probably due to massive gliosis of the optic nerve, so interpretation of protein expression data should be done with some caution. The process in this acute model resembles a fast-forward of changes in the chronic model of glaucoma. Therefore, impairment in axon transportation appears to be a common early process underlying different optic neuropathies. This research on effective intervention can be used to develop interventions for all optic neuropathies targeting axon transportation. |
doi_str_mv | 10.1007/s11427-019-1567-0 |
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In this study, we used a rat model of retinal ischemia-reperfusion and a one-time intravitreal brain-derived neurotrophic factor (BDNF) injection; then we examined axon transportation function, continuity, physical presence of axons in different part of the optic nerve, and the expression level of proteins involved in axon transportation. We found that in the disease model, axon transportation was the most severely affected, followed by axon continuity, then the number of axons in the distal and proximal optic nerve. BDNF treatment relieved all reductions and significantly restored function. The molecular changes were more minor, probably due to massive gliosis of the optic nerve, so interpretation of protein expression data should be done with some caution. The process in this acute model resembles a fast-forward of changes in the chronic model of glaucoma. Therefore, impairment in axon transportation appears to be a common early process underlying different optic neuropathies. This research on effective intervention can be used to develop interventions for all optic neuropathies targeting axon transportation.</description><identifier>ISSN: 1674-7305</identifier><identifier>EISSN: 1869-1889</identifier><identifier>DOI: 10.1007/s11427-019-1567-0</identifier><identifier>PMID: 32201927</identifier><language>eng</language><publisher>Beijing: Science China Press</publisher><subject>Animals ; Axonal Transport - drug effects ; Axons - drug effects ; Behavior Rating Scale ; Biomedical and Life Sciences ; Blindness ; Blindness - prevention & control ; Brain-derived neurotrophic factor ; Brain-Derived Neurotrophic Factor - administration & dosage ; Brain-Derived Neurotrophic Factor - metabolism ; Disease Models, Animal ; Glaucoma ; Glaucoma - metabolism ; Gliosis ; Injections, Intraocular ; Intraocular Pressure - drug effects ; Ischemia ; Life Sciences ; Male ; Neurodegeneration ; Optic nerve ; Optic Nerve - metabolism ; Protein transport ; Rats, Sprague-Dawley ; Reperfusion ; Research Paper ; Retina ; Retina - metabolism ; Retinal ganglion cells ; Retinal Ganglion Cells - metabolism ; Visual perception</subject><ispartof>Science China. Life sciences, 2020-09, Vol.63 (9), p.1337-1346</ispartof><rights>Science China Press and Springer-Verlag GmbH Germany, part of Springer Nature 2020</rights><rights>Science China Press and Springer-Verlag GmbH Germany, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-2bd3c13fe46ef53e71b76d372cddbf72be8a4605a48dfd4e6a9c68aa497498863</citedby><cites>FETCH-LOGICAL-c372t-2bd3c13fe46ef53e71b76d372cddbf72be8a4605a48dfd4e6a9c68aa497498863</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/s11427-019-1567-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11427-019-1567-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32201927$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Du, Rui</creatorcontrib><creatorcontrib>Wang, Xu</creatorcontrib><creatorcontrib>He, Shigang</creatorcontrib><title>BDNF improves axon transportation and rescues visual function in a rodent model of acute elevation of intraocular pressure</title><title>Science China. Life sciences</title><addtitle>Sci. China Life Sci</addtitle><addtitle>Sci China Life Sci</addtitle><description>Optic neuropathies lead to blindness; the common pathology is the degeneration of axons of the retinal ganglion cells. In this study, we used a rat model of retinal ischemia-reperfusion and a one-time intravitreal brain-derived neurotrophic factor (BDNF) injection; then we examined axon transportation function, continuity, physical presence of axons in different part of the optic nerve, and the expression level of proteins involved in axon transportation. We found that in the disease model, axon transportation was the most severely affected, followed by axon continuity, then the number of axons in the distal and proximal optic nerve. BDNF treatment relieved all reductions and significantly restored function. The molecular changes were more minor, probably due to massive gliosis of the optic nerve, so interpretation of protein expression data should be done with some caution. The process in this acute model resembles a fast-forward of changes in the chronic model of glaucoma. Therefore, impairment in axon transportation appears to be a common early process underlying different optic neuropathies. This research on effective intervention can be used to develop interventions for all optic neuropathies targeting axon transportation.</description><subject>Animals</subject><subject>Axonal Transport - drug effects</subject><subject>Axons - drug effects</subject><subject>Behavior Rating Scale</subject><subject>Biomedical and Life Sciences</subject><subject>Blindness</subject><subject>Blindness - prevention & control</subject><subject>Brain-derived neurotrophic factor</subject><subject>Brain-Derived Neurotrophic Factor - administration & dosage</subject><subject>Brain-Derived Neurotrophic Factor - metabolism</subject><subject>Disease Models, Animal</subject><subject>Glaucoma</subject><subject>Glaucoma - metabolism</subject><subject>Gliosis</subject><subject>Injections, Intraocular</subject><subject>Intraocular Pressure - drug effects</subject><subject>Ischemia</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Neurodegeneration</subject><subject>Optic nerve</subject><subject>Optic Nerve - metabolism</subject><subject>Protein transport</subject><subject>Rats, Sprague-Dawley</subject><subject>Reperfusion</subject><subject>Research Paper</subject><subject>Retina</subject><subject>Retina - metabolism</subject><subject>Retinal ganglion cells</subject><subject>Retinal Ganglion Cells - metabolism</subject><subject>Visual perception</subject><issn>1674-7305</issn><issn>1869-1889</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1UDtPwzAQthCIVqU_gAVZYg74FTsZoVBAqmCB2XJsB6VKk2AnFfDruZICE17uzt_jdB9Cp5RcUELUZaRUMJUQmic0ldAcoCnNJExZlh9CL5VIFCfpBM1jXBN4nBOm1DGacMZAx9QUfV7fPC5xtelCu_URm_e2wX0wTeza0Ju-gtE0Dgcf7QD4toqDqXE5NPYbqwDGoXW-6fEGSo3bEhs79B772m9HA_iqGjBt7VCbgDswi0PwJ-ioNHX0832doZfl7fPiPlk93T0srlaJ5Yr1CSsct5SXXkhfptwrWijpALLOFaVihc-MkCQ1InOlE16a3MrMGJErkWeZ5DN0PvrCjW9wRK_X7RAaWKmZ4CkjklMFLDqybGhjDL7UXag2JnxoSvQucD0GriE4vQtcE9Cc7Z2HYuPdr-InXiCwkRABal59-Fv9v-sX_fqNSw</recordid><startdate>20200901</startdate><enddate>20200901</enddate><creator>Du, Rui</creator><creator>Wang, Xu</creator><creator>He, Shigang</creator><general>Science China Press</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>7QP</scope><scope>7TK</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope></search><sort><creationdate>20200901</creationdate><title>BDNF improves axon transportation and rescues visual function in a rodent model of acute elevation of intraocular pressure</title><author>Du, Rui ; Wang, Xu ; He, Shigang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-2bd3c13fe46ef53e71b76d372cddbf72be8a4605a48dfd4e6a9c68aa497498863</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>Axonal Transport - drug effects</topic><topic>Axons - drug effects</topic><topic>Behavior Rating Scale</topic><topic>Biomedical and Life Sciences</topic><topic>Blindness</topic><topic>Blindness - prevention & control</topic><topic>Brain-derived neurotrophic factor</topic><topic>Brain-Derived Neurotrophic Factor - administration & dosage</topic><topic>Brain-Derived Neurotrophic Factor - metabolism</topic><topic>Disease Models, Animal</topic><topic>Glaucoma</topic><topic>Glaucoma - metabolism</topic><topic>Gliosis</topic><topic>Injections, Intraocular</topic><topic>Intraocular Pressure - drug effects</topic><topic>Ischemia</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Neurodegeneration</topic><topic>Optic nerve</topic><topic>Optic Nerve - metabolism</topic><topic>Protein transport</topic><topic>Rats, Sprague-Dawley</topic><topic>Reperfusion</topic><topic>Research Paper</topic><topic>Retina</topic><topic>Retina - metabolism</topic><topic>Retinal ganglion cells</topic><topic>Retinal Ganglion Cells - metabolism</topic><topic>Visual perception</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Du, Rui</creatorcontrib><creatorcontrib>Wang, Xu</creatorcontrib><creatorcontrib>He, Shigang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><jtitle>Science China. Life sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Du, Rui</au><au>Wang, Xu</au><au>He, Shigang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>BDNF improves axon transportation and rescues visual function in a rodent model of acute elevation of intraocular pressure</atitle><jtitle>Science China. Life sciences</jtitle><stitle>Sci. China Life Sci</stitle><addtitle>Sci China Life Sci</addtitle><date>2020-09-01</date><risdate>2020</risdate><volume>63</volume><issue>9</issue><spage>1337</spage><epage>1346</epage><pages>1337-1346</pages><issn>1674-7305</issn><eissn>1869-1889</eissn><abstract>Optic neuropathies lead to blindness; the common pathology is the degeneration of axons of the retinal ganglion cells. In this study, we used a rat model of retinal ischemia-reperfusion and a one-time intravitreal brain-derived neurotrophic factor (BDNF) injection; then we examined axon transportation function, continuity, physical presence of axons in different part of the optic nerve, and the expression level of proteins involved in axon transportation. We found that in the disease model, axon transportation was the most severely affected, followed by axon continuity, then the number of axons in the distal and proximal optic nerve. BDNF treatment relieved all reductions and significantly restored function. The molecular changes were more minor, probably due to massive gliosis of the optic nerve, so interpretation of protein expression data should be done with some caution. The process in this acute model resembles a fast-forward of changes in the chronic model of glaucoma. Therefore, impairment in axon transportation appears to be a common early process underlying different optic neuropathies. This research on effective intervention can be used to develop interventions for all optic neuropathies targeting axon transportation.</abstract><cop>Beijing</cop><pub>Science China Press</pub><pmid>32201927</pmid><doi>10.1007/s11427-019-1567-0</doi><tpages>10</tpages></addata></record> |
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subjects | Animals Axonal Transport - drug effects Axons - drug effects Behavior Rating Scale Biomedical and Life Sciences Blindness Blindness - prevention & control Brain-derived neurotrophic factor Brain-Derived Neurotrophic Factor - administration & dosage Brain-Derived Neurotrophic Factor - metabolism Disease Models, Animal Glaucoma Glaucoma - metabolism Gliosis Injections, Intraocular Intraocular Pressure - drug effects Ischemia Life Sciences Male Neurodegeneration Optic nerve Optic Nerve - metabolism Protein transport Rats, Sprague-Dawley Reperfusion Research Paper Retina Retina - metabolism Retinal ganglion cells Retinal Ganglion Cells - metabolism Visual perception |
title | BDNF improves axon transportation and rescues visual function in a rodent model of acute elevation of intraocular pressure |
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