Nerve Growth Factor Helps Protect Retina in Experimental Retinal Detachment
Purpose: To investigate the expression of nerve growth factor (NGF) and its receptor TrkA on the retina at different time points after retinal detachment (RD) and the protection effect of NGF in experimental RD. Methods: Sprague-Dawley rats were used as an RD animal model by injection of 0.1% sodium...
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| Veröffentlicht in: | Ophthalmologica (Basel) 2008-01, Vol.222 (1), p.58-61 |
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| creator | Sun, Xiaodong Xu, Xun Wang, Fenghua Zhang, Xi Ho, Patrick C.P. Liu, Haiyang Qian, Jin Yu, Zhang Lu, Hongfen Xu, Weiqi |
| description | Purpose: To investigate the expression of nerve growth factor (NGF) and its receptor TrkA on the retina at different time points after retinal detachment (RD) and the protection effect of NGF in experimental RD. Methods: Sprague-Dawley rats were used as an RD animal model by injection of 0.1% sodium hyaluronate under the neurosensory retina. The expression of endogenous NGF and its receptor TrkA in the rat retina was detected using immunohistochemistry. The NGF (5 µg/eye) or phosphate-buffered saline were injected separately into vitreous every 4 days after the RD. The rat eyes were then observed at various time points. Morphologic changes were investigated by light microscopy. Retinal gliosis was detected by glial fibrillary acidic protein labeling. Results: The expression of endogenous NGF and TrkA was upregulated during RD procedure. Most of the NGF-treated retina had a well-organized structure. In NGF-treated RD eyes, the cells were still significantly more numerous than in phosphate-buffered-saline-treated retina. Glial fibrillary acidic protein labeling increased quickly after RD; the NGF-treated retina had less reactive gliosis than the control groups. Conclusions: Intravitreal injection of exogenous NGF can protect retinal cells from degeneration in experimental RD. It may exert its protective action by preventing the apoptosis of retinal cells after RD. |
| doi_str_mv | 10.1159/000109281 |
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Methods: Sprague-Dawley rats were used as an RD animal model by injection of 0.1% sodium hyaluronate under the neurosensory retina. The expression of endogenous NGF and its receptor TrkA in the rat retina was detected using immunohistochemistry. The NGF (5 µg/eye) or phosphate-buffered saline were injected separately into vitreous every 4 days after the RD. The rat eyes were then observed at various time points. Morphologic changes were investigated by light microscopy. Retinal gliosis was detected by glial fibrillary acidic protein labeling. Results: The expression of endogenous NGF and TrkA was upregulated during RD procedure. Most of the NGF-treated retina had a well-organized structure. In NGF-treated RD eyes, the cells were still significantly more numerous than in phosphate-buffered-saline-treated retina. Glial fibrillary acidic protein labeling increased quickly after RD; the NGF-treated retina had less reactive gliosis than the control groups. Conclusions: Intravitreal injection of exogenous NGF can protect retinal cells from degeneration in experimental RD. It may exert its protective action by preventing the apoptosis of retinal cells after RD.</description><identifier>ISSN: 0030-3755</identifier><identifier>ISBN: 3805584555</identifier><identifier>ISBN: 9783805584555</identifier><identifier>EISSN: 1423-0267</identifier><identifier>EISBN: 3805584563</identifier><identifier>EISBN: 9783805584562</identifier><identifier>DOI: 10.1159/000109281</identifier><identifier>PMID: 18097183</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Animals ; Apoptosis - drug effects ; Glial Fibrillary Acidic Protein - metabolism ; Gliosis - pathology ; Injections ; Male ; Nerve Growth Factor - metabolism ; Nerve Growth Factor - pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptor, trkA - metabolism ; Recombinant Proteins - pharmacology ; Retina - drug effects ; Retina - pathology ; Retinal Degeneration - pathology ; Retinal Detachment - pathology ; Up-Regulation - physiology ; Vitreous Body</subject><ispartof>Ophthalmologica (Basel), 2008-01, Vol.222 (1), p.58-61</ispartof><rights>2007 S. Karger AG, Basel</rights><rights>(c) 2007 S. Karger AG, Basel.</rights><rights>Copyright (c) 2007 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c331t-acfa92a7b80cd675dcbab3a3e709ef1ab7b9e0849e33c692e02da23b162fb97d3</citedby><cites>FETCH-LOGICAL-c331t-acfa92a7b80cd675dcbab3a3e709ef1ab7b9e0849e33c692e02da23b162fb97d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,2423,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18097183$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sun, Xiaodong</creatorcontrib><creatorcontrib>Xu, Xun</creatorcontrib><creatorcontrib>Wang, Fenghua</creatorcontrib><creatorcontrib>Zhang, Xi</creatorcontrib><creatorcontrib>Ho, Patrick C.P.</creatorcontrib><creatorcontrib>Liu, Haiyang</creatorcontrib><creatorcontrib>Qian, Jin</creatorcontrib><creatorcontrib>Yu, Zhang</creatorcontrib><creatorcontrib>Lu, Hongfen</creatorcontrib><creatorcontrib>Xu, Weiqi</creatorcontrib><title>Nerve Growth Factor Helps Protect Retina in Experimental Retinal Detachment</title><title>Ophthalmologica (Basel)</title><addtitle>Ophthalmologica</addtitle><description>Purpose: To investigate the expression of nerve growth factor (NGF) and its receptor TrkA on the retina at different time points after retinal detachment (RD) and the protection effect of NGF in experimental RD. Methods: Sprague-Dawley rats were used as an RD animal model by injection of 0.1% sodium hyaluronate under the neurosensory retina. The expression of endogenous NGF and its receptor TrkA in the rat retina was detected using immunohistochemistry. The NGF (5 µg/eye) or phosphate-buffered saline were injected separately into vitreous every 4 days after the RD. The rat eyes were then observed at various time points. Morphologic changes were investigated by light microscopy. Retinal gliosis was detected by glial fibrillary acidic protein labeling. Results: The expression of endogenous NGF and TrkA was upregulated during RD procedure. Most of the NGF-treated retina had a well-organized structure. In NGF-treated RD eyes, the cells were still significantly more numerous than in phosphate-buffered-saline-treated retina. Glial fibrillary acidic protein labeling increased quickly after RD; the NGF-treated retina had less reactive gliosis than the control groups. Conclusions: Intravitreal injection of exogenous NGF can protect retinal cells from degeneration in experimental RD. It may exert its protective action by preventing the apoptosis of retinal cells after RD.</description><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Glial Fibrillary Acidic Protein - metabolism</subject><subject>Gliosis - pathology</subject><subject>Injections</subject><subject>Male</subject><subject>Nerve Growth Factor - metabolism</subject><subject>Nerve Growth Factor - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptor, trkA - metabolism</subject><subject>Recombinant Proteins - pharmacology</subject><subject>Retina - drug effects</subject><subject>Retina - pathology</subject><subject>Retinal Degeneration - pathology</subject><subject>Retinal Detachment - pathology</subject><subject>Up-Regulation - physiology</subject><subject>Vitreous Body</subject><issn>0030-3755</issn><issn>1423-0267</issn><isbn>3805584555</isbn><isbn>9783805584555</isbn><isbn>3805584563</isbn><isbn>9783805584562</isbn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkM1PwzAMxcOXYAwO3BGqOCBxKDhJ0zRHNAZDIEAIzlWaujDo1pGkfPz3ZKwCxMnS88_P9iNkh8IRpUIdAwAFxTK6RDZ5BkJkiUj5MunRhPEYWCpXfhtCrJIeAIeYSyE2yKZzz2FeKEXXyQbNQEma8R65vEb7htG5bd79U3SmjW9sNMJ65qJb23g0PrpDP57qaDyNhh8ztOMJTr2uO7mOTtFr8zQXt8hapWuH213tk4ez4f1gFF_dnF8MTq5iwzn1sTaVVkzLIgNTplKUptAF1xwlKKyoLmShELJEIecmVQyBlZrxgqasKpQseZ8cLHxntnlt0fl8MnYG61pPsWldzkBxpqQK4P4_8LlpbTg6MCwJ6xKRBehwARnbOGexymfhR20_cwr5PPj8J_jA7nWGbTHB8pfs8gzA7gJ40fYR7R-r7_kvTKqBiw</recordid><startdate>20080101</startdate><enddate>20080101</enddate><creator>Sun, Xiaodong</creator><creator>Xu, Xun</creator><creator>Wang, Fenghua</creator><creator>Zhang, Xi</creator><creator>Ho, Patrick C.P.</creator><creator>Liu, Haiyang</creator><creator>Qian, Jin</creator><creator>Yu, Zhang</creator><creator>Lu, Hongfen</creator><creator>Xu, Weiqi</creator><general>S. 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Lu, Hongfen ; Xu, Weiqi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c331t-acfa92a7b80cd675dcbab3a3e709ef1ab7b9e0849e33c692e02da23b162fb97d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Glial Fibrillary Acidic Protein - metabolism</topic><topic>Gliosis - pathology</topic><topic>Injections</topic><topic>Male</topic><topic>Nerve Growth Factor - metabolism</topic><topic>Nerve Growth Factor - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptor, trkA - metabolism</topic><topic>Recombinant Proteins - pharmacology</topic><topic>Retina - drug effects</topic><topic>Retina - pathology</topic><topic>Retinal Degeneration - pathology</topic><topic>Retinal Detachment - pathology</topic><topic>Up-Regulation - physiology</topic><topic>Vitreous Body</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sun, Xiaodong</creatorcontrib><creatorcontrib>Xu, Xun</creatorcontrib><creatorcontrib>Wang, Fenghua</creatorcontrib><creatorcontrib>Zhang, Xi</creatorcontrib><creatorcontrib>Ho, Patrick C.P.</creatorcontrib><creatorcontrib>Liu, Haiyang</creatorcontrib><creatorcontrib>Qian, Jin</creatorcontrib><creatorcontrib>Yu, Zhang</creatorcontrib><creatorcontrib>Lu, Hongfen</creatorcontrib><creatorcontrib>Xu, Weiqi</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>ProQuest Pharma Collection</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>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>Neurosciences Abstracts</collection><jtitle>Ophthalmologica (Basel)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sun, Xiaodong</au><au>Xu, Xun</au><au>Wang, Fenghua</au><au>Zhang, Xi</au><au>Ho, Patrick C.P.</au><au>Liu, Haiyang</au><au>Qian, Jin</au><au>Yu, Zhang</au><au>Lu, Hongfen</au><au>Xu, Weiqi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nerve Growth Factor Helps Protect Retina in Experimental Retinal Detachment</atitle><jtitle>Ophthalmologica (Basel)</jtitle><addtitle>Ophthalmologica</addtitle><date>2008-01-01</date><risdate>2008</risdate><volume>222</volume><issue>1</issue><spage>58</spage><epage>61</epage><pages>58-61</pages><issn>0030-3755</issn><eissn>1423-0267</eissn><isbn>3805584555</isbn><isbn>9783805584555</isbn><eisbn>3805584563</eisbn><eisbn>9783805584562</eisbn><abstract>Purpose: To investigate the expression of nerve growth factor (NGF) and its receptor TrkA on the retina at different time points after retinal detachment (RD) and the protection effect of NGF in experimental RD. Methods: Sprague-Dawley rats were used as an RD animal model by injection of 0.1% sodium hyaluronate under the neurosensory retina. The expression of endogenous NGF and its receptor TrkA in the rat retina was detected using immunohistochemistry. The NGF (5 µg/eye) or phosphate-buffered saline were injected separately into vitreous every 4 days after the RD. The rat eyes were then observed at various time points. Morphologic changes were investigated by light microscopy. Retinal gliosis was detected by glial fibrillary acidic protein labeling. Results: The expression of endogenous NGF and TrkA was upregulated during RD procedure. Most of the NGF-treated retina had a well-organized structure. In NGF-treated RD eyes, the cells were still significantly more numerous than in phosphate-buffered-saline-treated retina. Glial fibrillary acidic protein labeling increased quickly after RD; the NGF-treated retina had less reactive gliosis than the control groups. Conclusions: Intravitreal injection of exogenous NGF can protect retinal cells from degeneration in experimental RD. It may exert its protective action by preventing the apoptosis of retinal cells after RD.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>18097183</pmid><doi>10.1159/000109281</doi><tpages>4</tpages></addata></record> |
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| subjects | Animals Apoptosis - drug effects Glial Fibrillary Acidic Protein - metabolism Gliosis - pathology Injections Male Nerve Growth Factor - metabolism Nerve Growth Factor - pharmacology Rats Rats, Sprague-Dawley Receptor, trkA - metabolism Recombinant Proteins - pharmacology Retina - drug effects Retina - pathology Retinal Degeneration - pathology Retinal Detachment - pathology Up-Regulation - physiology Vitreous Body |
| title | Nerve Growth Factor Helps Protect Retina in Experimental Retinal Detachment |
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