Time-Dependent Nerve Growth Factor Signaling Changes in the Rat Retina During Optic Nerve Crush-Induced Degeneration of Retinal Ganglion Cells
Nerve growth factor (NGF) is suggested to be neuroprotective after nerve injury; however, retinal ganglion cells (RGC) degenerate following optic-nerve crush (ONC), even in the presence of increased levels of endogenous NGF. To further investigate this apparently paradoxical condition, a time-course...
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| Veröffentlicht in: | International journal of molecular sciences 2017-01, Vol.18 (1), p.98-98 |
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| creator | Mesentier-Louro, Louise A De Nicolò, Sara Rosso, Pamela De Vitis, Luigi A Castoldi, Valerio Leocani, Letizia Mendez-Otero, Rosalia Santiago, Marcelo F Tirassa, Paola Rama, Paolo Lambiase, Alessandro |
| description | Nerve growth factor (NGF) is suggested to be neuroprotective after nerve injury; however, retinal ganglion cells (RGC) degenerate following optic-nerve crush (ONC), even in the presence of increased levels of endogenous NGF. To further investigate this apparently paradoxical condition, a time-course study was performed to evaluate the effects of unilateral ONC on NGF expression and signaling in the adult retina. Visually evoked potential and immunofluorescence staining were used to assess axonal damage and RGC loss. The levels of NGF, proNGF, p75
, TrkA and GFAP and the activation of several intracellular pathways were analyzed at 1, 3, 7 and 14 days after crush (dac) by ELISA/Western Blot and PathScan intracellular signaling array. The progressive RGC loss and nerve impairment featured an early and sustained activation of apoptotic pathways; and GFAP and p75
enhancement. In contrast, ONC-induced reduction of TrkA, and increased proNGF were observed only at 7 and 14 dac. We propose that proNGF and p75
contribute to exacerbate retinal degeneration by further stimulating apoptosis during the second week after injury, and thus hamper the neuroprotective effect of the endogenous NGF. These findings might aid in identifying effective treatment windows for NGF-based strategies to counteract retinal and/or optic-nerve degeneration. |
| doi_str_mv | 10.3390/ijms18010098 |
| format | Article |
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, TrkA and GFAP and the activation of several intracellular pathways were analyzed at 1, 3, 7 and 14 days after crush (dac) by ELISA/Western Blot and PathScan intracellular signaling array. The progressive RGC loss and nerve impairment featured an early and sustained activation of apoptotic pathways; and GFAP and p75
enhancement. In contrast, ONC-induced reduction of TrkA, and increased proNGF were observed only at 7 and 14 dac. We propose that proNGF and p75
contribute to exacerbate retinal degeneration by further stimulating apoptosis during the second week after injury, and thus hamper the neuroprotective effect of the endogenous NGF. These findings might aid in identifying effective treatment windows for NGF-based strategies to counteract retinal and/or optic-nerve degeneration.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms18010098</identifier><identifier>PMID: 28067793</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Activation analysis ; Animals ; Apoptosis ; Blotting, Western ; Crush tests ; Damage assessment ; Degeneration ; Enzyme-linked immunosorbent assay ; Evoked Potentials, Visual - physiology ; Glial fibrillary acidic protein ; Glial Fibrillary Acidic Protein - metabolism ; Growth factors ; Immunofluorescence ; Intracellular ; Intracellular signalling ; Male ; Microscopy, Fluorescence ; Nerve Crush ; Nerve growth factor ; Nerve Growth Factor - metabolism ; Nerve Growth Factors - metabolism ; Nerve Tissue Proteins - metabolism ; Neuroprotection ; Optic nerve ; Optic Nerve Injuries - complications ; Protein Precursors - metabolism ; Rats ; Rats, Long-Evans ; Receptor, trkA - metabolism ; Receptors, Nerve Growth Factor - metabolism ; Retina ; Retina - metabolism ; Retina - physiopathology ; Retinal degeneration ; Retinal Degeneration - etiology ; Retinal Degeneration - metabolism ; Retinal Degeneration - physiopathology ; Retinal ganglion cells ; Retinal Ganglion Cells - metabolism ; Rodents ; Signal Transduction ; Staining ; Time Factors ; TrkA protein ; TrkA receptors</subject><ispartof>International journal of molecular sciences, 2017-01, Vol.18 (1), p.98-98</ispartof><rights>Copyright MDPI AG 2017</rights><rights>2017 by the authors; licensee MDPI, Basel, Switzerland. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c445t-62acff57f7b7a5dca4b1cf68e4fa1b0d3cf2f6f38090361ca0dc2785366a6bb73</citedby><cites>FETCH-LOGICAL-c445t-62acff57f7b7a5dca4b1cf68e4fa1b0d3cf2f6f38090361ca0dc2785366a6bb73</cites><orcidid>0000-0003-2428-9606 ; 0000-0002-8974-991X ; 0000-0003-3778-8666 ; 0000-0002-0937-9331</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5297732/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5297732/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28067793$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mesentier-Louro, Louise A</creatorcontrib><creatorcontrib>De Nicolò, Sara</creatorcontrib><creatorcontrib>Rosso, Pamela</creatorcontrib><creatorcontrib>De Vitis, Luigi A</creatorcontrib><creatorcontrib>Castoldi, Valerio</creatorcontrib><creatorcontrib>Leocani, Letizia</creatorcontrib><creatorcontrib>Mendez-Otero, Rosalia</creatorcontrib><creatorcontrib>Santiago, Marcelo F</creatorcontrib><creatorcontrib>Tirassa, Paola</creatorcontrib><creatorcontrib>Rama, Paolo</creatorcontrib><creatorcontrib>Lambiase, Alessandro</creatorcontrib><title>Time-Dependent Nerve Growth Factor Signaling Changes in the Rat Retina During Optic Nerve Crush-Induced Degeneration of Retinal Ganglion Cells</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Nerve growth factor (NGF) is suggested to be neuroprotective after nerve injury; however, retinal ganglion cells (RGC) degenerate following optic-nerve crush (ONC), even in the presence of increased levels of endogenous NGF. To further investigate this apparently paradoxical condition, a time-course study was performed to evaluate the effects of unilateral ONC on NGF expression and signaling in the adult retina. Visually evoked potential and immunofluorescence staining were used to assess axonal damage and RGC loss. The levels of NGF, proNGF, p75
, TrkA and GFAP and the activation of several intracellular pathways were analyzed at 1, 3, 7 and 14 days after crush (dac) by ELISA/Western Blot and PathScan intracellular signaling array. The progressive RGC loss and nerve impairment featured an early and sustained activation of apoptotic pathways; and GFAP and p75
enhancement. In contrast, ONC-induced reduction of TrkA, and increased proNGF were observed only at 7 and 14 dac. We propose that proNGF and p75
contribute to exacerbate retinal degeneration by further stimulating apoptosis during the second week after injury, and thus hamper the neuroprotective effect of the endogenous NGF. These findings might aid in identifying effective treatment windows for NGF-based strategies to counteract retinal and/or optic-nerve degeneration.</description><subject>Activation analysis</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Blotting, Western</subject><subject>Crush tests</subject><subject>Damage assessment</subject><subject>Degeneration</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Evoked Potentials, Visual - physiology</subject><subject>Glial fibrillary acidic protein</subject><subject>Glial Fibrillary Acidic Protein - metabolism</subject><subject>Growth factors</subject><subject>Immunofluorescence</subject><subject>Intracellular</subject><subject>Intracellular signalling</subject><subject>Male</subject><subject>Microscopy, Fluorescence</subject><subject>Nerve Crush</subject><subject>Nerve growth factor</subject><subject>Nerve Growth Factor - metabolism</subject><subject>Nerve Growth Factors - metabolism</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Neuroprotection</subject><subject>Optic nerve</subject><subject>Optic Nerve Injuries - complications</subject><subject>Protein Precursors - metabolism</subject><subject>Rats</subject><subject>Rats, Long-Evans</subject><subject>Receptor, trkA - metabolism</subject><subject>Receptors, Nerve Growth Factor - metabolism</subject><subject>Retina</subject><subject>Retina - metabolism</subject><subject>Retina - physiopathology</subject><subject>Retinal degeneration</subject><subject>Retinal Degeneration - etiology</subject><subject>Retinal Degeneration - metabolism</subject><subject>Retinal Degeneration - physiopathology</subject><subject>Retinal ganglion cells</subject><subject>Retinal Ganglion Cells - metabolism</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Staining</subject><subject>Time Factors</subject><subject>TrkA protein</subject><subject>TrkA receptors</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkk1v1DAQhi1ERUvhxhlZ4sKBUH8kjnNBqrJ0qVS1UinnyHHGiVeJvdhOEX-C30yWLtWWEydbM48fzVgvQm8o-ch5Rc7sZopUEkpIJZ-hE5ozlhEiyucH92P0MsYNIYyzonqBjplcimXFT9CvOztBtoItuA5cwtcQ7gGvg_-RBnyhdPIBf7W9U6N1Pa4H5XqI2DqcBsC3KuFbSNYpvJrDDrjZJqv3kjrMccguXTdr6PAKenAQVLLeYW_270a8XozjrlbDOMZX6MioMcLr_XmKvl18vqu_ZFc368v6_CrTeV6kTDCljSlKU7alKjqt8pZqIyTkRtGWdFwbZoThklSEC6oV6TQrZcGFUKJtS36KPj14t3M7QaeX1YMam22wkwo_G69s87Tj7ND0_r4pWFWWnC2C93tB8N9niKmZbNTLCsqBn2NDpZCc5ZSJ_0ALIUUuq91Y7_5BN34Oyzf9ETJKc17JhfrwQOngYwxgHuempNllojnMxIK_Pdz1Ef4bAv4b0jW0Zg</recordid><startdate>20170105</startdate><enddate>20170105</enddate><creator>Mesentier-Louro, Louise A</creator><creator>De Nicolò, Sara</creator><creator>Rosso, Pamela</creator><creator>De Vitis, Luigi A</creator><creator>Castoldi, Valerio</creator><creator>Leocani, Letizia</creator><creator>Mendez-Otero, Rosalia</creator><creator>Santiago, Marcelo F</creator><creator>Tirassa, Paola</creator><creator>Rama, Paolo</creator><creator>Lambiase, Alessandro</creator><general>MDPI AG</general><general>MDPI</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>7TK</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-2428-9606</orcidid><orcidid>https://orcid.org/0000-0002-8974-991X</orcidid><orcidid>https://orcid.org/0000-0003-3778-8666</orcidid><orcidid>https://orcid.org/0000-0002-0937-9331</orcidid></search><sort><creationdate>20170105</creationdate><title>Time-Dependent Nerve Growth Factor Signaling Changes in the Rat Retina During Optic Nerve Crush-Induced Degeneration of Retinal Ganglion Cells</title><author>Mesentier-Louro, Louise A ; De Nicolò, Sara ; Rosso, Pamela ; De Vitis, Luigi A ; Castoldi, Valerio ; Leocani, Letizia ; Mendez-Otero, Rosalia ; Santiago, Marcelo F ; Tirassa, Paola ; Rama, Paolo ; Lambiase, Alessandro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c445t-62acff57f7b7a5dca4b1cf68e4fa1b0d3cf2f6f38090361ca0dc2785366a6bb73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Activation analysis</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Blotting, Western</topic><topic>Crush tests</topic><topic>Damage assessment</topic><topic>Degeneration</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Evoked Potentials, Visual - physiology</topic><topic>Glial fibrillary acidic protein</topic><topic>Glial Fibrillary Acidic Protein - metabolism</topic><topic>Growth factors</topic><topic>Immunofluorescence</topic><topic>Intracellular</topic><topic>Intracellular signalling</topic><topic>Male</topic><topic>Microscopy, Fluorescence</topic><topic>Nerve Crush</topic><topic>Nerve growth factor</topic><topic>Nerve Growth Factor - metabolism</topic><topic>Nerve Growth Factors - metabolism</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Neuroprotection</topic><topic>Optic nerve</topic><topic>Optic Nerve Injuries - complications</topic><topic>Protein Precursors - metabolism</topic><topic>Rats</topic><topic>Rats, Long-Evans</topic><topic>Receptor, trkA - metabolism</topic><topic>Receptors, Nerve Growth Factor - metabolism</topic><topic>Retina</topic><topic>Retina - metabolism</topic><topic>Retina - physiopathology</topic><topic>Retinal degeneration</topic><topic>Retinal Degeneration - etiology</topic><topic>Retinal Degeneration - metabolism</topic><topic>Retinal Degeneration - physiopathology</topic><topic>Retinal ganglion cells</topic><topic>Retinal Ganglion Cells - metabolism</topic><topic>Rodents</topic><topic>Signal Transduction</topic><topic>Staining</topic><topic>Time Factors</topic><topic>TrkA protein</topic><topic>TrkA receptors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mesentier-Louro, Louise A</creatorcontrib><creatorcontrib>De Nicolò, Sara</creatorcontrib><creatorcontrib>Rosso, Pamela</creatorcontrib><creatorcontrib>De Vitis, Luigi A</creatorcontrib><creatorcontrib>Castoldi, Valerio</creatorcontrib><creatorcontrib>Leocani, Letizia</creatorcontrib><creatorcontrib>Mendez-Otero, Rosalia</creatorcontrib><creatorcontrib>Santiago, Marcelo F</creatorcontrib><creatorcontrib>Tirassa, Paola</creatorcontrib><creatorcontrib>Rama, Paolo</creatorcontrib><creatorcontrib>Lambiase, Alessandro</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</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 Central Basic</collection><collection>MEDLINE - 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To further investigate this apparently paradoxical condition, a time-course study was performed to evaluate the effects of unilateral ONC on NGF expression and signaling in the adult retina. Visually evoked potential and immunofluorescence staining were used to assess axonal damage and RGC loss. The levels of NGF, proNGF, p75
, TrkA and GFAP and the activation of several intracellular pathways were analyzed at 1, 3, 7 and 14 days after crush (dac) by ELISA/Western Blot and PathScan intracellular signaling array. The progressive RGC loss and nerve impairment featured an early and sustained activation of apoptotic pathways; and GFAP and p75
enhancement. In contrast, ONC-induced reduction of TrkA, and increased proNGF were observed only at 7 and 14 dac. We propose that proNGF and p75
contribute to exacerbate retinal degeneration by further stimulating apoptosis during the second week after injury, and thus hamper the neuroprotective effect of the endogenous NGF. These findings might aid in identifying effective treatment windows for NGF-based strategies to counteract retinal and/or optic-nerve degeneration.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>28067793</pmid><doi>10.3390/ijms18010098</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0003-2428-9606</orcidid><orcidid>https://orcid.org/0000-0002-8974-991X</orcidid><orcidid>https://orcid.org/0000-0003-3778-8666</orcidid><orcidid>https://orcid.org/0000-0002-0937-9331</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | International journal of molecular sciences, 2017-01, Vol.18 (1), p.98-98 |
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| source | MDPI - Multidisciplinary Digital Publishing Institute; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Activation analysis Animals Apoptosis Blotting, Western Crush tests Damage assessment Degeneration Enzyme-linked immunosorbent assay Evoked Potentials, Visual - physiology Glial fibrillary acidic protein Glial Fibrillary Acidic Protein - metabolism Growth factors Immunofluorescence Intracellular Intracellular signalling Male Microscopy, Fluorescence Nerve Crush Nerve growth factor Nerve Growth Factor - metabolism Nerve Growth Factors - metabolism Nerve Tissue Proteins - metabolism Neuroprotection Optic nerve Optic Nerve Injuries - complications Protein Precursors - metabolism Rats Rats, Long-Evans Receptor, trkA - metabolism Receptors, Nerve Growth Factor - metabolism Retina Retina - metabolism Retina - physiopathology Retinal degeneration Retinal Degeneration - etiology Retinal Degeneration - metabolism Retinal Degeneration - physiopathology Retinal ganglion cells Retinal Ganglion Cells - metabolism Rodents Signal Transduction Staining Time Factors TrkA protein TrkA receptors |
| title | Time-Dependent Nerve Growth Factor Signaling Changes in the Rat Retina During Optic Nerve Crush-Induced Degeneration of Retinal Ganglion Cells |
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