Loading…

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...

Full description

Saved in:
Bibliographic Details
Published in:Investigative ophthalmology & visual science 2013-02, Vol.54 (2), p.1280-1287
Main Authors: Kumar, Sandeep, Shah, Shaily, Deutsch, Emily Rose, Tang, Hai Michael, Danias, John
Format: Article
Language:English
Subjects:
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c387t-30bd0945278e99eb2ebefe437ecce3a0a652c9b5c097bba7c4570d5e03f1ce113
cites
container_end_page 1287
container_issue 2
container_start_page 1280
container_title Investigative ophthalmology & visual science
container_volume 54
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
format article
fullrecord <record><control><sourceid>pubmed_cross</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3576053</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>23322580</sourcerecordid><originalsourceid>FETCH-LOGICAL-c387t-30bd0945278e99eb2ebefe437ecce3a0a652c9b5c097bba7c4570d5e03f1ce113</originalsourceid><addsrcrecordid>eNpVkE1LAzEQhoMotlaPXiV_YNt8NJvdi6BFrVDwUs8hmZ3VyO6mJNtK_72t1aKnGZjnfQceQq45G3Oe64kPmzTmIuNcCHlChlwpkSldyNM_-4BcpPTBmNhR7JwMhJRCqIINyXwZvW3Bd6EJHVIL2IfOV0grhIg2YaJh3ddN-KS1Bd_4fkt9R2dK3y8mOW3DOiHFLaZLclbbJuHVzxyR18eH5WyeLV6enmd3iwxkoftMMlexcqqELrAs0Ql0WONUagRAaZnNlYDSKWClds5qmCrNKoVM1hyQczkit4fe1dq1WAF2fbSNWUXf2rg1wXrz_9L5d_MWNkYqnTMldwXZoQBiSClifcxyZvZKzV6p4cJ8K93xN38fHulfh_ILECJ0ag</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Triamcinolone acetonide decreases outflow facility in C57BL/6 mouse eyes</title><source>PubMed (Medline)</source><creator>Kumar, Sandeep ; Shah, Shaily ; Deutsch, Emily Rose ; Tang, Hai Michael ; Danias, John</creator><creatorcontrib>Kumar, Sandeep ; Shah, Shaily ; Deutsch, Emily Rose ; Tang, Hai Michael ; Danias, John</creatorcontrib><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 &lt; 0.01, P &lt; 0.001, respectively). Eyes treated with AA (with or without TA) had higher outflow facility than animals treated with TA (P &lt; 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 &lt; 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 &amp; 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 &amp; 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 &amp; 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 &lt; 0.01, P &lt; 0.001, respectively). Eyes treated with AA (with or without TA) had higher outflow facility than animals treated with TA (P &lt; 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 &lt; 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 &amp; 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 &amp; 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 &amp; 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 &amp; 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 &lt; 0.01, P &lt; 0.001, respectively). Eyes treated with AA (with or without TA) had higher outflow facility than animals treated with TA (P &lt; 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 &lt; 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>
fulltext fulltext
identifier ISSN: 1552-5783
ispartof Investigative ophthalmology & visual science, 2013-02, Vol.54 (2), p.1280-1287
issn 1552-5783
0146-0404
1552-5783
language eng
recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3576053
source PubMed (Medline)
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
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-26T23%3A51%3A04IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-pubmed_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Triamcinolone%20acetonide%20decreases%20outflow%20facility%20in%20C57BL/6%20mouse%20eyes&rft.jtitle=Investigative%20ophthalmology%20&%20visual%20science&rft.au=Kumar,%20Sandeep&rft.date=2013-02-01&rft.volume=54&rft.issue=2&rft.spage=1280&rft.epage=1287&rft.pages=1280-1287&rft.issn=1552-5783&rft.eissn=1552-5783&rft_id=info:doi/10.1167/iovs.12-11223&rft_dat=%3Cpubmed_cross%3E23322580%3C/pubmed_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c387t-30bd0945278e99eb2ebefe437ecce3a0a652c9b5c097bba7c4570d5e03f1ce113%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_id=info:pmid/23322580&rfr_iscdi=true