ACTH Increases Expression of c-fos, c-jun and β-actin Genes in the Dexamethasone-treated Rat Adrenals

Our recent finding that ACTH increases c-fos mRNA in the adrenal gland of hypophysectomized rats indicates that the gene product FOS may play an important role (s) in mediating the action of ACTH. However, hypophysectomy employed in that study causes the disappearance of trophic hormones other than...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Endocrinologia Japonica 1992, Vol.39(4), pp.377-383
Hauptverfasser: OHNO, MOTOTSUGU, SEO, HISAO, IMAI, TSUNEO, MURATA, YOSHIHARU, MIYAMOTO, NORIHIRO, SATOH, YASUYUKI, FUNAHASHI, HIROOMI, TAKAGI, HIROSHI, MATSUI, NOBUO
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 383
container_issue 4
container_start_page 377
container_title Endocrinologia Japonica
container_volume 39
creator OHNO, MOTOTSUGU
SEO, HISAO
IMAI, TSUNEO
MURATA, YOSHIHARU
MIYAMOTO, NORIHIRO
SATOH, YASUYUKI
FUNAHASHI, HIROOMI
TAKAGI, HIROSHI
MATSUI, NOBUO
description Our recent finding that ACTH increases c-fos mRNA in the adrenal gland of hypophysectomized rats indicates that the gene product FOS may play an important role (s) in mediating the action of ACTH. However, hypophysectomy employed in that study causes the disappearance of trophic hormones other than ACTH and may modify the effect of ACTH. Thus, in the present investigation, dexamethasone-treated rats were used. Since FOS functions only when it dimerizes with JUN (the product ofc-jun gene), the changes in the levels of c-fos and c-jun mRNAs were studied together with that of β-actin mRNA which is also affected by ACTH. Northern blot analysis was employed to determine the mRNA levels. It was demonstrated that ACTHincreases the mRNAs coding c-fos and c-jun in the adrenal glands of dexamethasone-treated, ACTH-suppressed rats. The c-fos mRNA was not detectable before ACTH administration. After ACTH administration, the mRNA levels were transiently increased, the maximum level being observed at 30min after ACTH. At 180min post ACTH, the level returned to the unstimulated level. The mRNA coding c-jun was detectable before ACTH administration and it also increased rapidly after ACTH with maximal stimulation at 30min. However, the mRNA level at 180min post ACTH was still higher than the unstimulated level. The changes in β-actin mRNA were approximately the same as those of c-jun mRNA. These results suggest that increased expression of c-fos, c-jun and β-actin genes by ACTH may play an important role in mediating its action on the adrenals.
doi_str_mv 10.1507/endocrj1954.39.377
format Article
fullrecord <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_73312831</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>73312831</sourcerecordid><originalsourceid>FETCH-LOGICAL-j231t-7e0013492c4c020f7e07484a65dfc5a824c5d7b70027f16e14e2d6473eb906ca3</originalsourceid><addsrcrecordid>eNpNkc9Kw0AQxhdRaql9AUHYg3gydf8lmxxLrVUQBNFzmG4mNiHd1N0t1NfyQXwmV6zFOcw3w_djmN0h5JyzCU-ZvkFb9ca1vEjVRBYTqfURGQqep0kmNTsmQ8a4TLTgxSkZe9-yGJnItGIDMuAiZ4KrIamns5d7-mCNQ_Do6Xy3ceh901va19Qkde-vo7RbS8FW9OszARMaSxdoIx2LsEJ6iztYY1iB7y0mIY4KWNFnCHRaObTQ-TNyUkfB8V5H5PVu_jK7Tx6fFg-z6WPSCslDovFnaVUIowwTrI69VrmCLK1qk0IulEkrvdSMCV3zDLlCUWVKS1wWLDMgR-Tqd-7G9e9b9KFcN95g14HFfutLLWV8uuQRvNiD2-Uaq3LjmjW4j3L_MdG_3PvgDXS1A2saf8CUEqKQecQWv1jrA7zhwQcXGtNh-e9IpSzKv6T1gTArcBGT354ljJE</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>73312831</pqid></control><display><type>article</type><title>ACTH Increases Expression of c-fos, c-jun and β-actin Genes in the Dexamethasone-treated Rat Adrenals</title><source>J-STAGE Free</source><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>OHNO, MOTOTSUGU ; SEO, HISAO ; IMAI, TSUNEO ; MURATA, YOSHIHARU ; MIYAMOTO, NORIHIRO ; SATOH, YASUYUKI ; FUNAHASHI, HIROOMI ; TAKAGI, HIROSHI ; MATSUI, NOBUO</creator><creatorcontrib>OHNO, MOTOTSUGU ; SEO, HISAO ; IMAI, TSUNEO ; MURATA, YOSHIHARU ; MIYAMOTO, NORIHIRO ; SATOH, YASUYUKI ; FUNAHASHI, HIROOMI ; TAKAGI, HIROSHI ; MATSUI, NOBUO</creatorcontrib><description>Our recent finding that ACTH increases c-fos mRNA in the adrenal gland of hypophysectomized rats indicates that the gene product FOS may play an important role (s) in mediating the action of ACTH. However, hypophysectomy employed in that study causes the disappearance of trophic hormones other than ACTH and may modify the effect of ACTH. Thus, in the present investigation, dexamethasone-treated rats were used. Since FOS functions only when it dimerizes with JUN (the product ofc-jun gene), the changes in the levels of c-fos and c-jun mRNAs were studied together with that of β-actin mRNA which is also affected by ACTH. Northern blot analysis was employed to determine the mRNA levels. It was demonstrated that ACTHincreases the mRNAs coding c-fos and c-jun in the adrenal glands of dexamethasone-treated, ACTH-suppressed rats. The c-fos mRNA was not detectable before ACTH administration. After ACTH administration, the mRNA levels were transiently increased, the maximum level being observed at 30min after ACTH. At 180min post ACTH, the level returned to the unstimulated level. The mRNA coding c-jun was detectable before ACTH administration and it also increased rapidly after ACTH with maximal stimulation at 30min. However, the mRNA level at 180min post ACTH was still higher than the unstimulated level. The changes in β-actin mRNA were approximately the same as those of c-jun mRNA. These results suggest that increased expression of c-fos, c-jun and β-actin genes by ACTH may play an important role in mediating its action on the adrenals.</description><identifier>ISSN: 0013-7219</identifier><identifier>EISSN: 2185-6370</identifier><identifier>DOI: 10.1507/endocrj1954.39.377</identifier><identifier>PMID: 1280214</identifier><identifier>CODEN: ECJPAE</identifier><language>eng</language><publisher>Tokyo: The Japan Endocrine Society</publisher><subject>ACTH ; Actins - genetics ; Adrenal Glands - drug effects ; Adrenals. Interrenals ; Adrenocortical hormones. Regulation ; Adrenocorticotropic Hormone - pharmacology ; Animals ; Biological and medical sciences ; c-fos ; c-jun ; Corticosterone - blood ; Dexamethasone - pharmacology ; DNA Probes ; Fundamental and applied biological sciences. Psychology ; Gene Expression Regulation - drug effects ; Genes, fos - genetics ; Genes, jun - genetics ; Male ; Rat adrenal ; Rats ; Rats, Wistar ; RNA - isolation &amp; purification ; RNA, Messenger - analysis ; Vertebrates: endocrinology ; β-Actin</subject><ispartof>Endocrinologia Japonica, 1992, Vol.39(4), pp.377-383</ispartof><rights>The Japan Endocrine Society</rights><rights>1993 INIST-CNRS</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1877,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=4422938$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1280214$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>OHNO, MOTOTSUGU</creatorcontrib><creatorcontrib>SEO, HISAO</creatorcontrib><creatorcontrib>IMAI, TSUNEO</creatorcontrib><creatorcontrib>MURATA, YOSHIHARU</creatorcontrib><creatorcontrib>MIYAMOTO, NORIHIRO</creatorcontrib><creatorcontrib>SATOH, YASUYUKI</creatorcontrib><creatorcontrib>FUNAHASHI, HIROOMI</creatorcontrib><creatorcontrib>TAKAGI, HIROSHI</creatorcontrib><creatorcontrib>MATSUI, NOBUO</creatorcontrib><title>ACTH Increases Expression of c-fos, c-jun and β-actin Genes in the Dexamethasone-treated Rat Adrenals</title><title>Endocrinologia Japonica</title><addtitle>Endocrinol Japon</addtitle><description>Our recent finding that ACTH increases c-fos mRNA in the adrenal gland of hypophysectomized rats indicates that the gene product FOS may play an important role (s) in mediating the action of ACTH. However, hypophysectomy employed in that study causes the disappearance of trophic hormones other than ACTH and may modify the effect of ACTH. Thus, in the present investigation, dexamethasone-treated rats were used. Since FOS functions only when it dimerizes with JUN (the product ofc-jun gene), the changes in the levels of c-fos and c-jun mRNAs were studied together with that of β-actin mRNA which is also affected by ACTH. Northern blot analysis was employed to determine the mRNA levels. It was demonstrated that ACTHincreases the mRNAs coding c-fos and c-jun in the adrenal glands of dexamethasone-treated, ACTH-suppressed rats. The c-fos mRNA was not detectable before ACTH administration. After ACTH administration, the mRNA levels were transiently increased, the maximum level being observed at 30min after ACTH. At 180min post ACTH, the level returned to the unstimulated level. The mRNA coding c-jun was detectable before ACTH administration and it also increased rapidly after ACTH with maximal stimulation at 30min. However, the mRNA level at 180min post ACTH was still higher than the unstimulated level. The changes in β-actin mRNA were approximately the same as those of c-jun mRNA. These results suggest that increased expression of c-fos, c-jun and β-actin genes by ACTH may play an important role in mediating its action on the adrenals.</description><subject>ACTH</subject><subject>Actins - genetics</subject><subject>Adrenal Glands - drug effects</subject><subject>Adrenals. Interrenals</subject><subject>Adrenocortical hormones. Regulation</subject><subject>Adrenocorticotropic Hormone - pharmacology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>c-fos</subject><subject>c-jun</subject><subject>Corticosterone - blood</subject><subject>Dexamethasone - pharmacology</subject><subject>DNA Probes</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Genes, fos - genetics</subject><subject>Genes, jun - genetics</subject><subject>Male</subject><subject>Rat adrenal</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>RNA - isolation &amp; purification</subject><subject>RNA, Messenger - analysis</subject><subject>Vertebrates: endocrinology</subject><subject>β-Actin</subject><issn>0013-7219</issn><issn>2185-6370</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkc9Kw0AQxhdRaql9AUHYg3gydf8lmxxLrVUQBNFzmG4mNiHd1N0t1NfyQXwmV6zFOcw3w_djmN0h5JyzCU-ZvkFb9ca1vEjVRBYTqfURGQqep0kmNTsmQ8a4TLTgxSkZe9-yGJnItGIDMuAiZ4KrIamns5d7-mCNQ_Do6Xy3ceh901va19Qkde-vo7RbS8FW9OszARMaSxdoIx2LsEJ6iztYY1iB7y0mIY4KWNFnCHRaObTQ-TNyUkfB8V5H5PVu_jK7Tx6fFg-z6WPSCslDovFnaVUIowwTrI69VrmCLK1qk0IulEkrvdSMCV3zDLlCUWVKS1wWLDMgR-Tqd-7G9e9b9KFcN95g14HFfutLLWV8uuQRvNiD2-Uaq3LjmjW4j3L_MdG_3PvgDXS1A2saf8CUEqKQecQWv1jrA7zhwQcXGtNh-e9IpSzKv6T1gTArcBGT354ljJE</recordid><startdate>19920801</startdate><enddate>19920801</enddate><creator>OHNO, MOTOTSUGU</creator><creator>SEO, HISAO</creator><creator>IMAI, TSUNEO</creator><creator>MURATA, YOSHIHARU</creator><creator>MIYAMOTO, NORIHIRO</creator><creator>SATOH, YASUYUKI</creator><creator>FUNAHASHI, HIROOMI</creator><creator>TAKAGI, HIROSHI</creator><creator>MATSUI, NOBUO</creator><general>The Japan Endocrine Society</general><general>Japan Endocrine Society</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>19920801</creationdate><title>ACTH Increases Expression of c-fos, c-jun and β-actin Genes in the Dexamethasone-treated Rat Adrenals</title><author>OHNO, MOTOTSUGU ; SEO, HISAO ; IMAI, TSUNEO ; MURATA, YOSHIHARU ; MIYAMOTO, NORIHIRO ; SATOH, YASUYUKI ; FUNAHASHI, HIROOMI ; TAKAGI, HIROSHI ; MATSUI, NOBUO</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-j231t-7e0013492c4c020f7e07484a65dfc5a824c5d7b70027f16e14e2d6473eb906ca3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1992</creationdate><topic>ACTH</topic><topic>Actins - genetics</topic><topic>Adrenal Glands - drug effects</topic><topic>Adrenals. Interrenals</topic><topic>Adrenocortical hormones. Regulation</topic><topic>Adrenocorticotropic Hormone - pharmacology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>c-fos</topic><topic>c-jun</topic><topic>Corticosterone - blood</topic><topic>Dexamethasone - pharmacology</topic><topic>DNA Probes</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Genes, fos - genetics</topic><topic>Genes, jun - genetics</topic><topic>Male</topic><topic>Rat adrenal</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>RNA - isolation &amp; purification</topic><topic>RNA, Messenger - analysis</topic><topic>Vertebrates: endocrinology</topic><topic>β-Actin</topic><toplevel>online_resources</toplevel><creatorcontrib>OHNO, MOTOTSUGU</creatorcontrib><creatorcontrib>SEO, HISAO</creatorcontrib><creatorcontrib>IMAI, TSUNEO</creatorcontrib><creatorcontrib>MURATA, YOSHIHARU</creatorcontrib><creatorcontrib>MIYAMOTO, NORIHIRO</creatorcontrib><creatorcontrib>SATOH, YASUYUKI</creatorcontrib><creatorcontrib>FUNAHASHI, HIROOMI</creatorcontrib><creatorcontrib>TAKAGI, HIROSHI</creatorcontrib><creatorcontrib>MATSUI, NOBUO</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>MEDLINE - Academic</collection><jtitle>Endocrinologia Japonica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>OHNO, MOTOTSUGU</au><au>SEO, HISAO</au><au>IMAI, TSUNEO</au><au>MURATA, YOSHIHARU</au><au>MIYAMOTO, NORIHIRO</au><au>SATOH, YASUYUKI</au><au>FUNAHASHI, HIROOMI</au><au>TAKAGI, HIROSHI</au><au>MATSUI, NOBUO</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ACTH Increases Expression of c-fos, c-jun and β-actin Genes in the Dexamethasone-treated Rat Adrenals</atitle><jtitle>Endocrinologia Japonica</jtitle><addtitle>Endocrinol Japon</addtitle><date>1992-08-01</date><risdate>1992</risdate><volume>39</volume><issue>4</issue><spage>377</spage><epage>383</epage><pages>377-383</pages><issn>0013-7219</issn><eissn>2185-6370</eissn><coden>ECJPAE</coden><abstract>Our recent finding that ACTH increases c-fos mRNA in the adrenal gland of hypophysectomized rats indicates that the gene product FOS may play an important role (s) in mediating the action of ACTH. However, hypophysectomy employed in that study causes the disappearance of trophic hormones other than ACTH and may modify the effect of ACTH. Thus, in the present investigation, dexamethasone-treated rats were used. Since FOS functions only when it dimerizes with JUN (the product ofc-jun gene), the changes in the levels of c-fos and c-jun mRNAs were studied together with that of β-actin mRNA which is also affected by ACTH. Northern blot analysis was employed to determine the mRNA levels. It was demonstrated that ACTHincreases the mRNAs coding c-fos and c-jun in the adrenal glands of dexamethasone-treated, ACTH-suppressed rats. The c-fos mRNA was not detectable before ACTH administration. After ACTH administration, the mRNA levels were transiently increased, the maximum level being observed at 30min after ACTH. At 180min post ACTH, the level returned to the unstimulated level. The mRNA coding c-jun was detectable before ACTH administration and it also increased rapidly after ACTH with maximal stimulation at 30min. However, the mRNA level at 180min post ACTH was still higher than the unstimulated level. The changes in β-actin mRNA were approximately the same as those of c-jun mRNA. These results suggest that increased expression of c-fos, c-jun and β-actin genes by ACTH may play an important role in mediating its action on the adrenals.</abstract><cop>Tokyo</cop><pub>The Japan Endocrine Society</pub><pmid>1280214</pmid><doi>10.1507/endocrj1954.39.377</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 0013-7219
ispartof Endocrinologia Japonica, 1992, Vol.39(4), pp.377-383
issn 0013-7219
2185-6370
language eng
recordid cdi_proquest_miscellaneous_73312831
source J-STAGE Free; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
subjects ACTH
Actins - genetics
Adrenal Glands - drug effects
Adrenals. Interrenals
Adrenocortical hormones. Regulation
Adrenocorticotropic Hormone - pharmacology
Animals
Biological and medical sciences
c-fos
c-jun
Corticosterone - blood
Dexamethasone - pharmacology
DNA Probes
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation - drug effects
Genes, fos - genetics
Genes, jun - genetics
Male
Rat adrenal
Rats
Rats, Wistar
RNA - isolation & purification
RNA, Messenger - analysis
Vertebrates: endocrinology
β-Actin
title ACTH Increases Expression of c-fos, c-jun and β-actin Genes in the Dexamethasone-treated Rat Adrenals
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-28T02%3A32%3A37IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=ACTH%20Increases%20Expression%20of%20c-fos,%20c-jun%20and%20%CE%B2-actin%20Genes%20in%20the%20Dexamethasone-treated%20Rat%20Adrenals&rft.jtitle=Endocrinologia%20Japonica&rft.au=OHNO,%20MOTOTSUGU&rft.date=1992-08-01&rft.volume=39&rft.issue=4&rft.spage=377&rft.epage=383&rft.pages=377-383&rft.issn=0013-7219&rft.eissn=2185-6370&rft.coden=ECJPAE&rft_id=info:doi/10.1507/endocrj1954.39.377&rft_dat=%3Cproquest_pubme%3E73312831%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=73312831&rft_id=info:pmid/1280214&rfr_iscdi=true