Altered gene expression profile in ovarian follicle in rats treated with indomethacin and RU486
It is well-known that indomethacin (the cyclooxygenase 1 & 2 inhibitor) and RU486 (or mifepristone, the progesterone receptor antagonist) block follicular rupture in rats. To characterize genetic alterations in unruptured follicles, gene expression profiles in ovarian follicle were analyzed in i...
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| Veröffentlicht in: | Journal of toxicological sciences 2015/06/01, Vol.40(3), pp.413-425 |
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| creator | Tsubota, Kenjiro Kanki, Masayuki Noto, Takahisa Nakatsuji, Shunji Oishi, Yuji Matsumoto, Masahiro Nakayama, Hiroyuki |
| description | It is well-known that indomethacin (the cyclooxygenase 1 & 2 inhibitor) and RU486 (or mifepristone, the progesterone receptor antagonist) block follicular rupture in rats. To characterize genetic alterations in unruptured follicles, gene expression profiles in ovarian follicle were analyzed in indomethacin- and RU486-treated female Sprague-Dawley rats. Ovaries are collected at 22:00 on the proestrus day and 10:00 on the following estrus day after a single dose of indomethacin and RU486. Histopathologically, changes depicting responses to LH surge were observed in ovaries, uteri and vagina. Total RNA was extracted from pre-ovulatory follicles or unruptured follicles collected by laser microdissection and analyzed by Genechip®. Among genes showing statistically significant changes compared to control groups, following changes were considered relevant to induction of unruptured follicles. In indomethacin-treated rats, Wnt4 was down-regulated, suggesting effect on tissue integrity and steroid genesis. In RU486-treated rats, Adamts1, Adamts9, Edn2, Ednra, Lyve1, Plat, and Pparg were down-regulated. These changes suggest effects on proteolysis for extra cellular matrix or surrounding tissue (Adamts1 & 9, and Plat), constriction of smooth muscle surrounding follicles (Edn2, Ednra, and Pparg), follicular fluid (Lyve1), and angiogenesis (Pparg). Down-regulation of angiogenesis related genes (Angpt2, Hmox1, and Vegfa) was observed in both treatment groups. Here, we clarify genetic alterations induced by the inhibition of cyclooxygenase or progesterone receptor. |
| doi_str_mv | 10.2131/jts.40.413 |
| format | Article |
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To characterize genetic alterations in unruptured follicles, gene expression profiles in ovarian follicle were analyzed in indomethacin- and RU486-treated female Sprague-Dawley rats. Ovaries are collected at 22:00 on the proestrus day and 10:00 on the following estrus day after a single dose of indomethacin and RU486. Histopathologically, changes depicting responses to LH surge were observed in ovaries, uteri and vagina. Total RNA was extracted from pre-ovulatory follicles or unruptured follicles collected by laser microdissection and analyzed by Genechip®. Among genes showing statistically significant changes compared to control groups, following changes were considered relevant to induction of unruptured follicles. In indomethacin-treated rats, Wnt4 was down-regulated, suggesting effect on tissue integrity and steroid genesis. In RU486-treated rats, Adamts1, Adamts9, Edn2, Ednra, Lyve1, Plat, and Pparg were down-regulated. These changes suggest effects on proteolysis for extra cellular matrix or surrounding tissue (Adamts1 & 9, and Plat), constriction of smooth muscle surrounding follicles (Edn2, Ednra, and Pparg), follicular fluid (Lyve1), and angiogenesis (Pparg). Down-regulation of angiogenesis related genes (Angpt2, Hmox1, and Vegfa) was observed in both treatment groups. Here, we clarify genetic alterations induced by the inhibition of cyclooxygenase or progesterone receptor.</description><identifier>ISSN: 0388-1350</identifier><identifier>EISSN: 1880-3989</identifier><identifier>DOI: 10.2131/jts.40.413</identifier><identifier>PMID: 25972201</identifier><language>eng</language><publisher>Japan: The Japanese Society of Toxicology</publisher><subject>Animals ; Cyclooxygenase Inhibitors - pharmacology ; Down-Regulation - drug effects ; Extracellular Matrix - metabolism ; Female ; Gene expression profiling ; Gene Expression Regulation, Developmental - drug effects ; Hormone Antagonists - pharmacology ; Indomethacin ; Indomethacin - pharmacology ; Mifepristone - pharmacology ; Neovascularization, Physiologic - drug effects ; Neovascularization, Physiologic - genetics ; Ovarian Follicle ; Proteolysis - drug effects ; Rats, Sprague-Dawley ; Receptors, Progesterone - antagonists & inhibitors ; RU486 ; Transcriptome - drug effects ; Unruptured follicle</subject><ispartof>The Journal of Toxicological Sciences, 2015/06/01, Vol.40(3), pp.413-425</ispartof><rights>2015 The Japanese Society of Toxicology</rights><rights>Copyright Japan Science and Technology Agency 2015</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c528t-3643b15bd871a609876760ebbc0c62a71f3d2ed47f4d493f098d24e65a2bdc4d3</citedby><cites>FETCH-LOGICAL-c528t-3643b15bd871a609876760ebbc0c62a71f3d2ed47f4d493f098d24e65a2bdc4d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1877,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25972201$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tsubota, Kenjiro</creatorcontrib><creatorcontrib>Kanki, Masayuki</creatorcontrib><creatorcontrib>Noto, Takahisa</creatorcontrib><creatorcontrib>Nakatsuji, Shunji</creatorcontrib><creatorcontrib>Oishi, Yuji</creatorcontrib><creatorcontrib>Matsumoto, Masahiro</creatorcontrib><creatorcontrib>Nakayama, Hiroyuki</creatorcontrib><title>Altered gene expression profile in ovarian follicle in rats treated with indomethacin and RU486</title><title>Journal of toxicological sciences</title><addtitle>J Toxicol Sci</addtitle><description>It is well-known that indomethacin (the cyclooxygenase 1 & 2 inhibitor) and RU486 (or mifepristone, the progesterone receptor antagonist) block follicular rupture in rats. To characterize genetic alterations in unruptured follicles, gene expression profiles in ovarian follicle were analyzed in indomethacin- and RU486-treated female Sprague-Dawley rats. Ovaries are collected at 22:00 on the proestrus day and 10:00 on the following estrus day after a single dose of indomethacin and RU486. Histopathologically, changes depicting responses to LH surge were observed in ovaries, uteri and vagina. Total RNA was extracted from pre-ovulatory follicles or unruptured follicles collected by laser microdissection and analyzed by Genechip®. Among genes showing statistically significant changes compared to control groups, following changes were considered relevant to induction of unruptured follicles. In indomethacin-treated rats, Wnt4 was down-regulated, suggesting effect on tissue integrity and steroid genesis. In RU486-treated rats, Adamts1, Adamts9, Edn2, Ednra, Lyve1, Plat, and Pparg were down-regulated. These changes suggest effects on proteolysis for extra cellular matrix or surrounding tissue (Adamts1 & 9, and Plat), constriction of smooth muscle surrounding follicles (Edn2, Ednra, and Pparg), follicular fluid (Lyve1), and angiogenesis (Pparg). Down-regulation of angiogenesis related genes (Angpt2, Hmox1, and Vegfa) was observed in both treatment groups. Here, we clarify genetic alterations induced by the inhibition of cyclooxygenase or progesterone receptor.</description><subject>Animals</subject><subject>Cyclooxygenase Inhibitors - pharmacology</subject><subject>Down-Regulation - drug effects</subject><subject>Extracellular Matrix - metabolism</subject><subject>Female</subject><subject>Gene expression profiling</subject><subject>Gene Expression Regulation, Developmental - drug effects</subject><subject>Hormone Antagonists - pharmacology</subject><subject>Indomethacin</subject><subject>Indomethacin - pharmacology</subject><subject>Mifepristone - pharmacology</subject><subject>Neovascularization, Physiologic - drug effects</subject><subject>Neovascularization, Physiologic - genetics</subject><subject>Ovarian Follicle</subject><subject>Proteolysis - drug effects</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Progesterone - antagonists & inhibitors</subject><subject>RU486</subject><subject>Transcriptome - drug effects</subject><subject>Unruptured follicle</subject><issn>0388-1350</issn><issn>1880-3989</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkctKAzEUhoMoWi8bH0AG3IgwNfdkFi5EvIEgiK5DJjljp0xnapJ6eXtTWrtw4yrw58vHOfkROiZ4TAkjF9MUxxyPOWFbaES0xiWrdLWNRphpXRIm8B7aj3GKMVVY8F20R0WlKMVkhMxVlyCAL96ghwK-5gFibIe-mIehaTso2r4YPmxobV80Q9e1bpUFm2KRAtiU3362aZJDP8wgTazL17b3xfMr1_IQ7TS2i3C0Pg_Q6-3Ny_V9-fh093B99Vg6QXUqmeSsJqL2WhErcaWVVBJDXTvsJLWKNMxT8Fw13POKNZnwlIMUltbecc8O0NnKm-d-X0BMZtZGB11nexgW0RAlRVVRJuT_qNSESq64yujpH3Q6LEKfF8lCIXSeUy-F5yvKhSHGAI2Zh3Zmw7ch2CwbMrkhw7HJDWX4ZK1c1DPwG_S3kgxcroBpTPYNNoANafn5vy62Fm5yN7HBQM9-AKhCoRs</recordid><startdate>20150601</startdate><enddate>20150601</enddate><creator>Tsubota, Kenjiro</creator><creator>Kanki, Masayuki</creator><creator>Noto, Takahisa</creator><creator>Nakatsuji, Shunji</creator><creator>Oishi, Yuji</creator><creator>Matsumoto, Masahiro</creator><creator>Nakayama, Hiroyuki</creator><general>The Japanese Society of Toxicology</general><general>Japan Science and Technology Agency</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>7ST</scope><scope>7U7</scope><scope>C1K</scope><scope>SOI</scope><scope>7X8</scope></search><sort><creationdate>20150601</creationdate><title>Altered gene expression profile in ovarian follicle in rats treated with indomethacin and RU486</title><author>Tsubota, Kenjiro ; Kanki, Masayuki ; Noto, Takahisa ; Nakatsuji, Shunji ; Oishi, Yuji ; Matsumoto, Masahiro ; Nakayama, Hiroyuki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c528t-3643b15bd871a609876760ebbc0c62a71f3d2ed47f4d493f098d24e65a2bdc4d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Cyclooxygenase Inhibitors - pharmacology</topic><topic>Down-Regulation - drug effects</topic><topic>Extracellular Matrix - metabolism</topic><topic>Female</topic><topic>Gene expression profiling</topic><topic>Gene Expression Regulation, Developmental - drug effects</topic><topic>Hormone Antagonists - pharmacology</topic><topic>Indomethacin</topic><topic>Indomethacin - pharmacology</topic><topic>Mifepristone - pharmacology</topic><topic>Neovascularization, Physiologic - drug effects</topic><topic>Neovascularization, Physiologic - genetics</topic><topic>Ovarian Follicle</topic><topic>Proteolysis - drug effects</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Progesterone - antagonists & inhibitors</topic><topic>RU486</topic><topic>Transcriptome - drug effects</topic><topic>Unruptured follicle</topic><toplevel>online_resources</toplevel><creatorcontrib>Tsubota, Kenjiro</creatorcontrib><creatorcontrib>Kanki, Masayuki</creatorcontrib><creatorcontrib>Noto, Takahisa</creatorcontrib><creatorcontrib>Nakatsuji, Shunji</creatorcontrib><creatorcontrib>Oishi, Yuji</creatorcontrib><creatorcontrib>Matsumoto, Masahiro</creatorcontrib><creatorcontrib>Nakayama, Hiroyuki</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Environment Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Environment Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of toxicological sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tsubota, Kenjiro</au><au>Kanki, Masayuki</au><au>Noto, Takahisa</au><au>Nakatsuji, Shunji</au><au>Oishi, Yuji</au><au>Matsumoto, Masahiro</au><au>Nakayama, Hiroyuki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Altered gene expression profile in ovarian follicle in rats treated with indomethacin and RU486</atitle><jtitle>Journal of toxicological sciences</jtitle><addtitle>J Toxicol Sci</addtitle><date>2015-06-01</date><risdate>2015</risdate><volume>40</volume><issue>3</issue><spage>413</spage><epage>425</epage><pages>413-425</pages><issn>0388-1350</issn><eissn>1880-3989</eissn><abstract>It is well-known that indomethacin (the cyclooxygenase 1 & 2 inhibitor) and RU486 (or mifepristone, the progesterone receptor antagonist) block follicular rupture in rats. To characterize genetic alterations in unruptured follicles, gene expression profiles in ovarian follicle were analyzed in indomethacin- and RU486-treated female Sprague-Dawley rats. Ovaries are collected at 22:00 on the proestrus day and 10:00 on the following estrus day after a single dose of indomethacin and RU486. Histopathologically, changes depicting responses to LH surge were observed in ovaries, uteri and vagina. Total RNA was extracted from pre-ovulatory follicles or unruptured follicles collected by laser microdissection and analyzed by Genechip®. Among genes showing statistically significant changes compared to control groups, following changes were considered relevant to induction of unruptured follicles. In indomethacin-treated rats, Wnt4 was down-regulated, suggesting effect on tissue integrity and steroid genesis. In RU486-treated rats, Adamts1, Adamts9, Edn2, Ednra, Lyve1, Plat, and Pparg were down-regulated. These changes suggest effects on proteolysis for extra cellular matrix or surrounding tissue (Adamts1 & 9, and Plat), constriction of smooth muscle surrounding follicles (Edn2, Ednra, and Pparg), follicular fluid (Lyve1), and angiogenesis (Pparg). Down-regulation of angiogenesis related genes (Angpt2, Hmox1, and Vegfa) was observed in both treatment groups. Here, we clarify genetic alterations induced by the inhibition of cyclooxygenase or progesterone receptor.</abstract><cop>Japan</cop><pub>The Japanese Society of Toxicology</pub><pmid>25972201</pmid><doi>10.2131/jts.40.413</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Cyclooxygenase Inhibitors - pharmacology Down-Regulation - drug effects Extracellular Matrix - metabolism Female Gene expression profiling Gene Expression Regulation, Developmental - drug effects Hormone Antagonists - pharmacology Indomethacin Indomethacin - pharmacology Mifepristone - pharmacology Neovascularization, Physiologic - drug effects Neovascularization, Physiologic - genetics Ovarian Follicle Proteolysis - drug effects Rats, Sprague-Dawley Receptors, Progesterone - antagonists & inhibitors RU486 Transcriptome - drug effects Unruptured follicle |
| title | Altered gene expression profile in ovarian follicle in rats treated with indomethacin and RU486 |
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