Nerve Growth Factor Role on Retinal Ganglion Cell Survival and Axon Regrowth: Effects of Ocular Administration in Experimental Model of Optic Nerve Injury
Retinal ganglion cell (RGC) degeneration occurs within 2 weeks following optic nerve crush (ONC) as a consequence of reduced retro-transport of growth factors including nerve growth factor (NGF). The hypothesis that intravitreal (ivt) and eye drop (ed) administration of recombinant human NGF (rhNGF)...
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| Veröffentlicht in: | Molecular neurobiology 2019-02, Vol.56 (2), p.1056-1069 |
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| creator | Mesentier-Louro, Louise A. Rosso, Pamela Carito, Valentina Mendez-Otero, Rosalia Santiago, Marcelo F. Rama, Paolo Lambiase, Alessandro Tirassa, Paola |
| description | Retinal ganglion cell (RGC) degeneration occurs within 2 weeks following optic nerve crush (ONC) as a consequence of reduced retro-transport of growth factors including nerve growth factor (NGF). The hypothesis that intravitreal (ivt) and eye drop (ed) administration of recombinant human NGF (rhNGF) might counteract ONC in adult rats is explored in this study. We found that both ivt- and ed-rhNGF reduced RGC loss and stimulated axonal regrowth. Chiefly, survival and regenerative effects of rhNGF were associated with a reduction of cells co-expressing Nogo-A/p75NTR at crush site borders, which contribute to glia scar formation following nerve injury, and induce further degeneration. We also found that ocular application of rhNGF reduced p75NTR and proNGF and enhanced phosphorylation of TrkA and its intracellular signals at retina level. Nogo-R and Rock2 expression was also normalized by ed-rhNGF treatment in both ONC and contralateral retina. Our findings that ocular applied NGF reaches and exerts biological actions on posterior segment of the eye give a further insight into the neurotrophin diffusion/transport through eye structures and/or their trafficking in optic nerve. In addition, the use of a highly purified NGF form in injury condition in which proNGF/p75NTR binding is favored indicates that increased availability of mature NGF restores the balance between TrkA and p75NGF, thus resulting in RGC survival and axonal growth. In conclusion, ocular applied NGF is confirmed as a good experimental paradigm to study mechanisms of neurodegeneration and regeneration, disclose biomarkers, and time windows for efficacy treatment following cell or nerve injury. |
| doi_str_mv | 10.1007/s12035-018-1154-1 |
| format | Article |
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The hypothesis that intravitreal (ivt) and eye drop (ed) administration of recombinant human NGF (rhNGF) might counteract ONC in adult rats is explored in this study. We found that both ivt- and ed-rhNGF reduced RGC loss and stimulated axonal regrowth. Chiefly, survival and regenerative effects of rhNGF were associated with a reduction of cells co-expressing Nogo-A/p75NTR at crush site borders, which contribute to glia scar formation following nerve injury, and induce further degeneration. We also found that ocular application of rhNGF reduced p75NTR and proNGF and enhanced phosphorylation of TrkA and its intracellular signals at retina level. Nogo-R and Rock2 expression was also normalized by ed-rhNGF treatment in both ONC and contralateral retina. Our findings that ocular applied NGF reaches and exerts biological actions on posterior segment of the eye give a further insight into the neurotrophin diffusion/transport through eye structures and/or their trafficking in optic nerve. In addition, the use of a highly purified NGF form in injury condition in which proNGF/p75NTR binding is favored indicates that increased availability of mature NGF restores the balance between TrkA and p75NGF, thus resulting in RGC survival and axonal growth. In conclusion, ocular applied NGF is confirmed as a good experimental paradigm to study mechanisms of neurodegeneration and regeneration, disclose biomarkers, and time windows for efficacy treatment following cell or nerve injury.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-018-1154-1</identifier><identifier>PMID: 29869196</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Cell survival ; Cell Survival - drug effects ; Eye ; Growth factors ; Male ; Models, Theoretical ; Nerve growth factor ; Nerve Growth Factor - pharmacology ; Neurobiology ; Neurodegeneration ; Neurology ; Neurosciences ; Nogo protein ; Nogo Proteins - metabolism ; Optic nerve ; Optic Nerve - drug effects ; Optic Nerve Injuries - chemically induced ; Optic Nerve Injuries - drug therapy ; Phosphorylation ; Rats, Long-Evans ; Regeneration ; Regrowth ; Retina ; Retina - metabolism ; Retinal ganglion cells ; Retinal Ganglion Cells - drug effects ; Retinal Ganglion Cells - metabolism ; TrkA protein ; TrkA receptors</subject><ispartof>Molecular neurobiology, 2019-02, Vol.56 (2), p.1056-1069</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2018</rights><rights>Molecular Neurobiology is a copyright of Springer, (2018). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c438t-81818c5ed16ebe2e640986edad96464a8f009e2230f4192d4c5f8556b64ac96a3</citedby><cites>FETCH-LOGICAL-c438t-81818c5ed16ebe2e640986edad96464a8f009e2230f4192d4c5f8556b64ac96a3</cites><orcidid>0000-0002-8791-4424</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/s12035-018-1154-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-018-1154-1$$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/29869196$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mesentier-Louro, Louise A.</creatorcontrib><creatorcontrib>Rosso, Pamela</creatorcontrib><creatorcontrib>Carito, Valentina</creatorcontrib><creatorcontrib>Mendez-Otero, Rosalia</creatorcontrib><creatorcontrib>Santiago, Marcelo F.</creatorcontrib><creatorcontrib>Rama, Paolo</creatorcontrib><creatorcontrib>Lambiase, Alessandro</creatorcontrib><creatorcontrib>Tirassa, Paola</creatorcontrib><title>Nerve Growth Factor Role on Retinal Ganglion Cell Survival and Axon Regrowth: Effects of Ocular Administration in Experimental Model of Optic Nerve Injury</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><addtitle>Mol Neurobiol</addtitle><description>Retinal ganglion cell (RGC) degeneration occurs within 2 weeks following optic nerve crush (ONC) as a consequence of reduced retro-transport of growth factors including nerve growth factor (NGF). The hypothesis that intravitreal (ivt) and eye drop (ed) administration of recombinant human NGF (rhNGF) might counteract ONC in adult rats is explored in this study. We found that both ivt- and ed-rhNGF reduced RGC loss and stimulated axonal regrowth. Chiefly, survival and regenerative effects of rhNGF were associated with a reduction of cells co-expressing Nogo-A/p75NTR at crush site borders, which contribute to glia scar formation following nerve injury, and induce further degeneration. We also found that ocular application of rhNGF reduced p75NTR and proNGF and enhanced phosphorylation of TrkA and its intracellular signals at retina level. Nogo-R and Rock2 expression was also normalized by ed-rhNGF treatment in both ONC and contralateral retina. Our findings that ocular applied NGF reaches and exerts biological actions on posterior segment of the eye give a further insight into the neurotrophin diffusion/transport through eye structures and/or their trafficking in optic nerve. In addition, the use of a highly purified NGF form in injury condition in which proNGF/p75NTR binding is favored indicates that increased availability of mature NGF restores the balance between TrkA and p75NGF, thus resulting in RGC survival and axonal growth. In conclusion, ocular applied NGF is confirmed as a good experimental paradigm to study mechanisms of neurodegeneration and regeneration, disclose biomarkers, and time windows for efficacy treatment following cell or nerve injury.</description><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Cell survival</subject><subject>Cell Survival - drug effects</subject><subject>Eye</subject><subject>Growth factors</subject><subject>Male</subject><subject>Models, Theoretical</subject><subject>Nerve growth factor</subject><subject>Nerve Growth Factor - pharmacology</subject><subject>Neurobiology</subject><subject>Neurodegeneration</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Nogo protein</subject><subject>Nogo Proteins - metabolism</subject><subject>Optic nerve</subject><subject>Optic Nerve - drug effects</subject><subject>Optic Nerve Injuries - chemically 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Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mesentier-Louro, Louise A.</au><au>Rosso, Pamela</au><au>Carito, Valentina</au><au>Mendez-Otero, Rosalia</au><au>Santiago, Marcelo F.</au><au>Rama, Paolo</au><au>Lambiase, Alessandro</au><au>Tirassa, Paola</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nerve Growth Factor Role on Retinal Ganglion Cell Survival and Axon Regrowth: Effects of Ocular Administration in Experimental Model of Optic Nerve Injury</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><addtitle>Mol Neurobiol</addtitle><date>2019-02-01</date><risdate>2019</risdate><volume>56</volume><issue>2</issue><spage>1056</spage><epage>1069</epage><pages>1056-1069</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>Retinal ganglion cell (RGC) degeneration occurs within 2 weeks following optic nerve crush (ONC) as a consequence of reduced retro-transport of growth factors including nerve growth factor (NGF). The hypothesis that intravitreal (ivt) and eye drop (ed) administration of recombinant human NGF (rhNGF) might counteract ONC in adult rats is explored in this study. We found that both ivt- and ed-rhNGF reduced RGC loss and stimulated axonal regrowth. Chiefly, survival and regenerative effects of rhNGF were associated with a reduction of cells co-expressing Nogo-A/p75NTR at crush site borders, which contribute to glia scar formation following nerve injury, and induce further degeneration. We also found that ocular application of rhNGF reduced p75NTR and proNGF and enhanced phosphorylation of TrkA and its intracellular signals at retina level. Nogo-R and Rock2 expression was also normalized by ed-rhNGF treatment in both ONC and contralateral retina. Our findings that ocular applied NGF reaches and exerts biological actions on posterior segment of the eye give a further insight into the neurotrophin diffusion/transport through eye structures and/or their trafficking in optic nerve. In addition, the use of a highly purified NGF form in injury condition in which proNGF/p75NTR binding is favored indicates that increased availability of mature NGF restores the balance between TrkA and p75NGF, thus resulting in RGC survival and axonal growth. In conclusion, ocular applied NGF is confirmed as a good experimental paradigm to study mechanisms of neurodegeneration and regeneration, disclose biomarkers, and time windows for efficacy treatment following cell or nerve injury.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>29869196</pmid><doi>10.1007/s12035-018-1154-1</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-8791-4424</orcidid></addata></record> |
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| subjects | Animals Biomedical and Life Sciences Biomedicine Cell Biology Cell survival Cell Survival - drug effects Eye Growth factors Male Models, Theoretical Nerve growth factor Nerve Growth Factor - pharmacology Neurobiology Neurodegeneration Neurology Neurosciences Nogo protein Nogo Proteins - metabolism Optic nerve Optic Nerve - drug effects Optic Nerve Injuries - chemically induced Optic Nerve Injuries - drug therapy Phosphorylation Rats, Long-Evans Regeneration Regrowth Retina Retina - metabolism Retinal ganglion cells Retinal Ganglion Cells - drug effects Retinal Ganglion Cells - metabolism TrkA protein TrkA receptors |
| title | Nerve Growth Factor Role on Retinal Ganglion Cell Survival and Axon Regrowth: Effects of Ocular Administration in Experimental Model of Optic Nerve Injury |
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