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Triamcinolone acetonide decreases outflow facility in C57BL/6 mouse eyes
To determine the effect of triamcinolone acetonide (TA) on outflow facility in mice. Animals received 20 μL of TA (40 mg/mL) suspension subconjunctivally either bilaterally or unilaterally and were euthanized after either 1 week or 3 weeks. Before mice were killed, IOP was measured with a rebound to...
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Published in: | Investigative ophthalmology & visual science 2013-02, Vol.54 (2), p.1280-1287 |
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creator | Kumar, Sandeep Shah, Shaily Deutsch, Emily Rose Tang, Hai Michael Danias, John |
description | To determine the effect of triamcinolone acetonide (TA) on outflow facility in mice.
Animals received 20 μL of TA (40 mg/mL) suspension subconjunctivally either bilaterally or unilaterally and were euthanized after either 1 week or 3 weeks. Before mice were killed, IOP was measured with a rebound tonometer. Outflow facility was determined using simultaneous pressure and flow measurements. Another set of animals received bilateral injection of anecortave acetate (AA) with or without bilateral TA injection and their outflow facility was also determined. Myocilin expression was investigated in a subset of eyes using quantitative PCR (qPCR).
Outflow facility of eyes in animals receiving bilateral TA injection (TA(BL)) and TA-treated eyes of animals receiving unilateral injection (TA(UL)) was significantly decreased compared to naïve control eyes (C(naive)) after 1 week and 3 weeks of TA treatment (ANOVA P < 0.01, P < 0.001, respectively). Eyes treated with AA (with or without TA) had higher outflow facility than animals treated with TA (P < 0.05). IOP data did not show any significant difference between groups. qPCR analysis revealed significant decrease in myocilin expression in eyes receiving AA compared to naïve control and TA-treated eyes (ANOVA P < 0.001).
Steroid treatment significantly decreases outflow facility in C57BL/6 mice despite having small effect on IOP. This animal model can be useful for studying the pathogenesis of steroid-induced glaucoma. |
doi_str_mv | 10.1167/iovs.12-11223 |
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Animals received 20 μL of TA (40 mg/mL) suspension subconjunctivally either bilaterally or unilaterally and were euthanized after either 1 week or 3 weeks. Before mice were killed, IOP was measured with a rebound tonometer. Outflow facility was determined using simultaneous pressure and flow measurements. Another set of animals received bilateral injection of anecortave acetate (AA) with or without bilateral TA injection and their outflow facility was also determined. Myocilin expression was investigated in a subset of eyes using quantitative PCR (qPCR).
Outflow facility of eyes in animals receiving bilateral TA injection (TA(BL)) and TA-treated eyes of animals receiving unilateral injection (TA(UL)) was significantly decreased compared to naïve control eyes (C(naive)) after 1 week and 3 weeks of TA treatment (ANOVA P < 0.01, P < 0.001, respectively). Eyes treated with AA (with or without TA) had higher outflow facility than animals treated with TA (P < 0.05). IOP data did not show any significant difference between groups. qPCR analysis revealed significant decrease in myocilin expression in eyes receiving AA compared to naïve control and TA-treated eyes (ANOVA P < 0.001).
Steroid treatment significantly decreases outflow facility in C57BL/6 mice despite having small effect on IOP. This animal model can be useful for studying the pathogenesis of steroid-induced glaucoma.</description><identifier>ISSN: 1552-5783</identifier><identifier>ISSN: 0146-0404</identifier><identifier>EISSN: 1552-5783</identifier><identifier>DOI: 10.1167/iovs.12-11223</identifier><identifier>PMID: 23322580</identifier><language>eng</language><publisher>United States: The Association for Research in Vision and Ophthalmology</publisher><subject>Animals ; Cytoskeletal Proteins - genetics ; Cytoskeletal Proteins - metabolism ; Disease Models, Animal ; Eye Proteins - genetics ; Eye Proteins - metabolism ; Female ; Glaucoma - chemically induced ; Glaucoma - metabolism ; Glucocorticoids - toxicity ; Glycoproteins - genetics ; Glycoproteins - metabolism ; Hydrocortisone - analogs & derivatives ; Hydrocortisone - toxicity ; Intraocular Pressure - drug effects ; Intraocular Pressure - physiology ; Mice ; Mice, Inbred C57BL ; Microdialysis - methods ; Models, Biological ; RNA, Messenger - metabolism ; Trabecular Meshwork - drug effects ; Trabecular Meshwork - metabolism ; Triamcinolone Acetonide - toxicity</subject><ispartof>Investigative ophthalmology & visual science, 2013-02, Vol.54 (2), p.1280-1287</ispartof><rights>Copyright 2013 The Association for Research in Vision and Ophthalmology, Inc. 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c387t-30bd0945278e99eb2ebefe437ecce3a0a652c9b5c097bba7c4570d5e03f1ce113</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3576053/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3576053/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23322580$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kumar, Sandeep</creatorcontrib><creatorcontrib>Shah, Shaily</creatorcontrib><creatorcontrib>Deutsch, Emily Rose</creatorcontrib><creatorcontrib>Tang, Hai Michael</creatorcontrib><creatorcontrib>Danias, John</creatorcontrib><title>Triamcinolone acetonide decreases outflow facility in C57BL/6 mouse eyes</title><title>Investigative ophthalmology & visual science</title><addtitle>Invest Ophthalmol Vis Sci</addtitle><description>To determine the effect of triamcinolone acetonide (TA) on outflow facility in mice.
Animals received 20 μL of TA (40 mg/mL) suspension subconjunctivally either bilaterally or unilaterally and were euthanized after either 1 week or 3 weeks. Before mice were killed, IOP was measured with a rebound tonometer. Outflow facility was determined using simultaneous pressure and flow measurements. Another set of animals received bilateral injection of anecortave acetate (AA) with or without bilateral TA injection and their outflow facility was also determined. Myocilin expression was investigated in a subset of eyes using quantitative PCR (qPCR).
Outflow facility of eyes in animals receiving bilateral TA injection (TA(BL)) and TA-treated eyes of animals receiving unilateral injection (TA(UL)) was significantly decreased compared to naïve control eyes (C(naive)) after 1 week and 3 weeks of TA treatment (ANOVA P < 0.01, P < 0.001, respectively). Eyes treated with AA (with or without TA) had higher outflow facility than animals treated with TA (P < 0.05). IOP data did not show any significant difference between groups. qPCR analysis revealed significant decrease in myocilin expression in eyes receiving AA compared to naïve control and TA-treated eyes (ANOVA P < 0.001).
Steroid treatment significantly decreases outflow facility in C57BL/6 mice despite having small effect on IOP. This animal model can be useful for studying the pathogenesis of steroid-induced glaucoma.</description><subject>Animals</subject><subject>Cytoskeletal Proteins - genetics</subject><subject>Cytoskeletal Proteins - metabolism</subject><subject>Disease Models, Animal</subject><subject>Eye Proteins - genetics</subject><subject>Eye Proteins - metabolism</subject><subject>Female</subject><subject>Glaucoma - chemically induced</subject><subject>Glaucoma - metabolism</subject><subject>Glucocorticoids - toxicity</subject><subject>Glycoproteins - genetics</subject><subject>Glycoproteins - metabolism</subject><subject>Hydrocortisone - analogs & derivatives</subject><subject>Hydrocortisone - toxicity</subject><subject>Intraocular Pressure - drug effects</subject><subject>Intraocular Pressure - physiology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Microdialysis - methods</subject><subject>Models, Biological</subject><subject>RNA, Messenger - metabolism</subject><subject>Trabecular Meshwork - drug effects</subject><subject>Trabecular Meshwork - metabolism</subject><subject>Triamcinolone Acetonide - toxicity</subject><issn>1552-5783</issn><issn>0146-0404</issn><issn>1552-5783</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNpVkE1LAzEQhoMotlaPXiV_YNt8NJvdi6BFrVDwUs8hmZ3VyO6mJNtK_72t1aKnGZjnfQceQq45G3Oe64kPmzTmIuNcCHlChlwpkSldyNM_-4BcpPTBmNhR7JwMhJRCqIINyXwZvW3Bd6EJHVIL2IfOV0grhIg2YaJh3ddN-KS1Bd_4fkt9R2dK3y8mOW3DOiHFLaZLclbbJuHVzxyR18eH5WyeLV6enmd3iwxkoftMMlexcqqELrAs0Ql0WONUagRAaZnNlYDSKWClds5qmCrNKoVM1hyQczkit4fe1dq1WAF2fbSNWUXf2rg1wXrz_9L5d_MWNkYqnTMldwXZoQBiSClifcxyZvZKzV6p4cJ8K93xN38fHulfh_ILECJ0ag</recordid><startdate>20130201</startdate><enddate>20130201</enddate><creator>Kumar, Sandeep</creator><creator>Shah, Shaily</creator><creator>Deutsch, Emily Rose</creator><creator>Tang, Hai Michael</creator><creator>Danias, John</creator><general>The Association for Research in Vision and Ophthalmology</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>5PM</scope></search><sort><creationdate>20130201</creationdate><title>Triamcinolone acetonide decreases outflow facility in C57BL/6 mouse eyes</title><author>Kumar, Sandeep ; Shah, Shaily ; Deutsch, Emily Rose ; Tang, Hai Michael ; Danias, John</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c387t-30bd0945278e99eb2ebefe437ecce3a0a652c9b5c097bba7c4570d5e03f1ce113</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Cytoskeletal Proteins - genetics</topic><topic>Cytoskeletal Proteins - metabolism</topic><topic>Disease Models, Animal</topic><topic>Eye Proteins - genetics</topic><topic>Eye Proteins - metabolism</topic><topic>Female</topic><topic>Glaucoma - chemically induced</topic><topic>Glaucoma - metabolism</topic><topic>Glucocorticoids - toxicity</topic><topic>Glycoproteins - genetics</topic><topic>Glycoproteins - metabolism</topic><topic>Hydrocortisone - analogs & derivatives</topic><topic>Hydrocortisone - toxicity</topic><topic>Intraocular Pressure - drug effects</topic><topic>Intraocular Pressure - physiology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Microdialysis - methods</topic><topic>Models, Biological</topic><topic>RNA, Messenger - metabolism</topic><topic>Trabecular Meshwork - drug effects</topic><topic>Trabecular Meshwork - metabolism</topic><topic>Triamcinolone Acetonide - toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kumar, Sandeep</creatorcontrib><creatorcontrib>Shah, Shaily</creatorcontrib><creatorcontrib>Deutsch, Emily Rose</creatorcontrib><creatorcontrib>Tang, Hai Michael</creatorcontrib><creatorcontrib>Danias, John</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Investigative ophthalmology & visual science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kumar, Sandeep</au><au>Shah, Shaily</au><au>Deutsch, Emily Rose</au><au>Tang, Hai Michael</au><au>Danias, John</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Triamcinolone acetonide decreases outflow facility in C57BL/6 mouse eyes</atitle><jtitle>Investigative ophthalmology & visual science</jtitle><addtitle>Invest Ophthalmol Vis Sci</addtitle><date>2013-02-01</date><risdate>2013</risdate><volume>54</volume><issue>2</issue><spage>1280</spage><epage>1287</epage><pages>1280-1287</pages><issn>1552-5783</issn><issn>0146-0404</issn><eissn>1552-5783</eissn><abstract>To determine the effect of triamcinolone acetonide (TA) on outflow facility in mice.
Animals received 20 μL of TA (40 mg/mL) suspension subconjunctivally either bilaterally or unilaterally and were euthanized after either 1 week or 3 weeks. Before mice were killed, IOP was measured with a rebound tonometer. Outflow facility was determined using simultaneous pressure and flow measurements. Another set of animals received bilateral injection of anecortave acetate (AA) with or without bilateral TA injection and their outflow facility was also determined. Myocilin expression was investigated in a subset of eyes using quantitative PCR (qPCR).
Outflow facility of eyes in animals receiving bilateral TA injection (TA(BL)) and TA-treated eyes of animals receiving unilateral injection (TA(UL)) was significantly decreased compared to naïve control eyes (C(naive)) after 1 week and 3 weeks of TA treatment (ANOVA P < 0.01, P < 0.001, respectively). Eyes treated with AA (with or without TA) had higher outflow facility than animals treated with TA (P < 0.05). IOP data did not show any significant difference between groups. qPCR analysis revealed significant decrease in myocilin expression in eyes receiving AA compared to naïve control and TA-treated eyes (ANOVA P < 0.001).
Steroid treatment significantly decreases outflow facility in C57BL/6 mice despite having small effect on IOP. This animal model can be useful for studying the pathogenesis of steroid-induced glaucoma.</abstract><cop>United States</cop><pub>The Association for Research in Vision and Ophthalmology</pub><pmid>23322580</pmid><doi>10.1167/iovs.12-11223</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Cytoskeletal Proteins - genetics Cytoskeletal Proteins - metabolism Disease Models, Animal Eye Proteins - genetics Eye Proteins - metabolism Female Glaucoma - chemically induced Glaucoma - metabolism Glucocorticoids - toxicity Glycoproteins - genetics Glycoproteins - metabolism Hydrocortisone - analogs & derivatives Hydrocortisone - toxicity Intraocular Pressure - drug effects Intraocular Pressure - physiology Mice Mice, Inbred C57BL Microdialysis - methods Models, Biological RNA, Messenger - metabolism Trabecular Meshwork - drug effects Trabecular Meshwork - metabolism Triamcinolone Acetonide - toxicity |
title | Triamcinolone acetonide decreases outflow facility in C57BL/6 mouse eyes |
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