Change in endothelial nitric oxide synthase in the rat retina following transient ischemia
Patterns of endothelial nitric oxide synthase (eNOS) expression in retinal ischemia were studied utilizing a transient high intraocular pressure (HIOP) model. We investigated neuronal cell damage and changes in eNOS immunoreactive expression in the ischemic retina, and its relationship to the neurop...
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| Veröffentlicht in: | Neuroreport 2003-03, Vol.14 (3), p.329-333 |
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| creator | Cheon, Eun Woo Park, Chang Hwan Kang, Sang Soo Cho, Gyeong Jae Yoo, Ji Myong Song, Joon Kyung Choi, Wan Sung |
| description | Patterns of endothelial nitric oxide synthase (eNOS) expression in retinal ischemia were studied utilizing a transient high intraocular pressure (HIOP) model. We investigated neuronal cell damage and changes in eNOS immunoreactive expression in the ischemic retina, and its relationship to the neuroprotection of betaxolol treatment after ischemic injury. Immunohistochemical staining for eNOS was performed at 3, 7, 14 and 28 days after ischemia/reperfusion. In controls, eNOS immunoreactivity was detected in retinal vessels, but was not detected in neurons. After ischemia/reperfusion, the intensity of eNOS immunoreactivity increased in both retinal vessels and the ganglion cell layer (GCL) compared with controls. eNOS-positive neurons were induced first in the inner nuclear layer (INL) 7 days after reperfusion. However, when experiments were carried out on animals that had been treated with betaxolol after ischemia/reperfusion, the intensity of eNOS immunoreactivity decreased compared to the untreated ischemic retinas. These results suggest that an increase in eNOS expression could be associated with the degenerative changes in the ischemic retina, and that betaxolol treatment appears to protect retinal tissue from ischemic damage. |
| doi_str_mv | 10.1097/00001756-200303030-00007 |
| format | Article |
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We investigated neuronal cell damage and changes in eNOS immunoreactive expression in the ischemic retina, and its relationship to the neuroprotection of betaxolol treatment after ischemic injury. Immunohistochemical staining for eNOS was performed at 3, 7, 14 and 28 days after ischemia/reperfusion. In controls, eNOS immunoreactivity was detected in retinal vessels, but was not detected in neurons. After ischemia/reperfusion, the intensity of eNOS immunoreactivity increased in both retinal vessels and the ganglion cell layer (GCL) compared with controls. eNOS-positive neurons were induced first in the inner nuclear layer (INL) 7 days after reperfusion. However, when experiments were carried out on animals that had been treated with betaxolol after ischemia/reperfusion, the intensity of eNOS immunoreactivity decreased compared to the untreated ischemic retinas. These results suggest that an increase in eNOS expression could be associated with the degenerative changes in the ischemic retina, and that betaxolol treatment appears to protect retinal tissue from ischemic damage.</description><identifier>ISSN: 0959-4965</identifier><identifier>EISSN: 1473-558X</identifier><identifier>DOI: 10.1097/00001756-200303030-00007</identifier><identifier>PMID: 12634478</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins, Inc</publisher><subject>Administration, Topical ; Adrenergic beta-Antagonists - administration & dosage ; Animals ; Betaxolol - administration & dosage ; Biological and medical sciences ; Ischemia - enzymology ; Ischemia - pathology ; Male ; Medical sciences ; Neuroprotective Agents - administration & dosage ; Nitric Oxide Synthase - antagonists & inhibitors ; Nitric Oxide Synthase - metabolism ; Nitric Oxide Synthase Type III ; Ophthalmology ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury - enzymology ; Reperfusion Injury - pathology ; Retina - enzymology ; Retina - pathology ; Retinal Vessels ; Retinopathies</subject><ispartof>Neuroreport, 2003-03, Vol.14 (3), p.329-333</ispartof><rights>2003 Lippincott Williams & Wilkins, Inc.</rights><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3987-1705cb5bd7a8ad9ecb3b6ee4ac0453b336c05a67a116e3f4a1d8521bc005e9ee3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27929,27930</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14669802$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12634478$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cheon, Eun Woo</creatorcontrib><creatorcontrib>Park, Chang Hwan</creatorcontrib><creatorcontrib>Kang, Sang Soo</creatorcontrib><creatorcontrib>Cho, Gyeong Jae</creatorcontrib><creatorcontrib>Yoo, Ji Myong</creatorcontrib><creatorcontrib>Song, Joon Kyung</creatorcontrib><creatorcontrib>Choi, Wan Sung</creatorcontrib><title>Change in endothelial nitric oxide synthase in the rat retina following transient ischemia</title><title>Neuroreport</title><addtitle>Neuroreport</addtitle><description>Patterns of endothelial nitric oxide synthase (eNOS) expression in retinal ischemia were studied utilizing a transient high intraocular pressure (HIOP) model. We investigated neuronal cell damage and changes in eNOS immunoreactive expression in the ischemic retina, and its relationship to the neuroprotection of betaxolol treatment after ischemic injury. Immunohistochemical staining for eNOS was performed at 3, 7, 14 and 28 days after ischemia/reperfusion. In controls, eNOS immunoreactivity was detected in retinal vessels, but was not detected in neurons. After ischemia/reperfusion, the intensity of eNOS immunoreactivity increased in both retinal vessels and the ganglion cell layer (GCL) compared with controls. eNOS-positive neurons were induced first in the inner nuclear layer (INL) 7 days after reperfusion. However, when experiments were carried out on animals that had been treated with betaxolol after ischemia/reperfusion, the intensity of eNOS immunoreactivity decreased compared to the untreated ischemic retinas. These results suggest that an increase in eNOS expression could be associated with the degenerative changes in the ischemic retina, and that betaxolol treatment appears to protect retinal tissue from ischemic damage.</description><subject>Administration, Topical</subject><subject>Adrenergic beta-Antagonists - administration & dosage</subject><subject>Animals</subject><subject>Betaxolol - administration & dosage</subject><subject>Biological and medical sciences</subject><subject>Ischemia - enzymology</subject><subject>Ischemia - pathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Neuroprotective Agents - administration & dosage</subject><subject>Nitric Oxide Synthase - antagonists & inhibitors</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Nitric Oxide Synthase Type III</subject><subject>Ophthalmology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reperfusion Injury - enzymology</subject><subject>Reperfusion Injury - pathology</subject><subject>Retina - enzymology</subject><subject>Retina - pathology</subject><subject>Retinal Vessels</subject><subject>Retinopathies</subject><issn>0959-4965</issn><issn>1473-558X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0kuPFCEQAGBiNO64-hcMF721QvNqjmbiK9nEiybGC6mmq7dRhl6Bybj_XnZmdE9GOJBUvqJIFYRQzl5xZs1r1hY3Snc9Y-K4u7uQeUA2XBrRKTV8fUg2zCrbSavVBXlSyvcmLOPDY3LBey2kNMOGfNsukK6RhkQxTWtdMAaINIWag6frrzAhLbepLlCOqAGaodKMNSSg8xrjegjpmtYMqQRMlYbiF9wFeEoezRALPjufl-TLu7eftx-6q0_vP27fXHVe2MF03DDlRzVOBgaYLPpRjBpRgmdSiVEI7ZkCbYBzjWKWwKdB9Xz0jCm0iOKSvDzde5PXn3ss1e3aEzBGSLjuizOCs0EY_l_YM8VYz2WDwwn6vJaScXY3Oewg3zrO3N0A3J8BuL8DOIZMS31-rrEfdzjdJ5473sCLM4DiIc6tbT6Ueye1tgPrm5Mnd1hjxVx-xP0Bs1sQYl3cvz6A-A0-lJ38</recordid><startdate>20030303</startdate><enddate>20030303</enddate><creator>Cheon, Eun Woo</creator><creator>Park, Chang Hwan</creator><creator>Kang, Sang Soo</creator><creator>Cho, Gyeong Jae</creator><creator>Yoo, Ji Myong</creator><creator>Song, Joon Kyung</creator><creator>Choi, Wan Sung</creator><general>Lippincott Williams & Wilkins, Inc</general><general>Lippincott Williams and Wilkins</general><scope>IQODW</scope><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>7TK</scope><scope>7X8</scope></search><sort><creationdate>20030303</creationdate><title>Change in endothelial nitric oxide synthase in the rat retina following transient ischemia</title><author>Cheon, Eun Woo ; Park, Chang Hwan ; Kang, Sang Soo ; Cho, Gyeong Jae ; Yoo, Ji Myong ; Song, Joon Kyung ; Choi, Wan Sung</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3987-1705cb5bd7a8ad9ecb3b6ee4ac0453b336c05a67a116e3f4a1d8521bc005e9ee3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Administration, Topical</topic><topic>Adrenergic beta-Antagonists - administration & dosage</topic><topic>Animals</topic><topic>Betaxolol - administration & dosage</topic><topic>Biological and medical sciences</topic><topic>Ischemia - enzymology</topic><topic>Ischemia - pathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Neuroprotective Agents - administration & dosage</topic><topic>Nitric Oxide Synthase - antagonists & inhibitors</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Nitric Oxide Synthase Type III</topic><topic>Ophthalmology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reperfusion Injury - enzymology</topic><topic>Reperfusion Injury - pathology</topic><topic>Retina - enzymology</topic><topic>Retina - pathology</topic><topic>Retinal Vessels</topic><topic>Retinopathies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cheon, Eun Woo</creatorcontrib><creatorcontrib>Park, Chang Hwan</creatorcontrib><creatorcontrib>Kang, Sang Soo</creatorcontrib><creatorcontrib>Cho, Gyeong Jae</creatorcontrib><creatorcontrib>Yoo, Ji Myong</creatorcontrib><creatorcontrib>Song, Joon Kyung</creatorcontrib><creatorcontrib>Choi, Wan Sung</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neuroreport</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cheon, Eun Woo</au><au>Park, Chang Hwan</au><au>Kang, Sang Soo</au><au>Cho, Gyeong Jae</au><au>Yoo, Ji Myong</au><au>Song, Joon Kyung</au><au>Choi, Wan Sung</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Change in endothelial nitric oxide synthase in the rat retina following transient ischemia</atitle><jtitle>Neuroreport</jtitle><addtitle>Neuroreport</addtitle><date>2003-03-03</date><risdate>2003</risdate><volume>14</volume><issue>3</issue><spage>329</spage><epage>333</epage><pages>329-333</pages><issn>0959-4965</issn><eissn>1473-558X</eissn><abstract>Patterns of endothelial nitric oxide synthase (eNOS) expression in retinal ischemia were studied utilizing a transient high intraocular pressure (HIOP) model. We investigated neuronal cell damage and changes in eNOS immunoreactive expression in the ischemic retina, and its relationship to the neuroprotection of betaxolol treatment after ischemic injury. Immunohistochemical staining for eNOS was performed at 3, 7, 14 and 28 days after ischemia/reperfusion. In controls, eNOS immunoreactivity was detected in retinal vessels, but was not detected in neurons. After ischemia/reperfusion, the intensity of eNOS immunoreactivity increased in both retinal vessels and the ganglion cell layer (GCL) compared with controls. eNOS-positive neurons were induced first in the inner nuclear layer (INL) 7 days after reperfusion. However, when experiments were carried out on animals that had been treated with betaxolol after ischemia/reperfusion, the intensity of eNOS immunoreactivity decreased compared to the untreated ischemic retinas. These results suggest that an increase in eNOS expression could be associated with the degenerative changes in the ischemic retina, and that betaxolol treatment appears to protect retinal tissue from ischemic damage.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins, Inc</pub><pmid>12634478</pmid><doi>10.1097/00001756-200303030-00007</doi><tpages>5</tpages></addata></record> |
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| subjects | Administration, Topical Adrenergic beta-Antagonists - administration & dosage Animals Betaxolol - administration & dosage Biological and medical sciences Ischemia - enzymology Ischemia - pathology Male Medical sciences Neuroprotective Agents - administration & dosage Nitric Oxide Synthase - antagonists & inhibitors Nitric Oxide Synthase - metabolism Nitric Oxide Synthase Type III Ophthalmology Rats Rats, Sprague-Dawley Reperfusion Injury - enzymology Reperfusion Injury - pathology Retina - enzymology Retina - pathology Retinal Vessels Retinopathies |
| title | Change in endothelial nitric oxide synthase in the rat retina following transient ischemia |
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