Selective Roles of Retinoic Acid Receptor and Retinoid X Receptor in the Suppression of Apoptosis by All-trans-retinoic Acid
Retinoic acids exert profound effects on many biological processes including cell proliferation, differentiation, and morphogenesis. We previously reported that all- trans -retinoic acid (t-RA) protected mesangial cells from H 2 O 2 -triggered apoptosis by suppressing the activator protein 1 (AP-1)...
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creator | Konta, T Xu, Q Furusu, A Nakayama, K Kitamura, M |
description | Retinoic acids exert profound effects on many biological processes including cell proliferation, differentiation, and morphogenesis.
We previously reported that all- trans -retinoic acid (t-RA) protected mesangial cells from H 2 O 2 -triggered apoptosis by suppressing the activator protein 1 (AP-1) pathway. It was via inhibition of c- fos and c- jun expression and suppression of c-Jun N-terminal kinase (JNK) activation. In this report, we investigated the involvement of
retinoic acid receptor (RAR) and retinoid X receptor (RXR) in the antiapoptotic effect of t-RA in H 2 O 2 -exposed cells. We found that pretreatment with RAR pan-antagonist (AGN193109) or RXR pan-antagonist (HX531) attenuated the
antiapoptotic effect of t-RA. Similarly, transient transfection with a dominant-negative mutant of RAR or a dominant-negative
RXR diminished the antiapoptotic effect of t-RA. Both RAR and RXR antagonists reversed the suppressive effect of t-RA on AP-1
activity. However, the roles of RAR and RXR in the suppression of AP-1 components by t-RA were found to be different. RAR
antagonist reversed the suppressive effect of t-RA on both c- fos and c- jun , whereas RXR antagonist reversed the effect of t-RA on c- fos but not c- jun . Furthermore, suppression of JNK activation by t-RA was observed even in the presence of RAR and RXR antagonists. Consistently,
suppression of JNK by t-RA was not affected by overexpression of either the dominant-negative RAR or the dominant-negative
RXR. These data elucidated that the antiapoptotic effect of t-RA is mediated by both nuclear receptor-dependent and -independent
mechanisms. |
doi_str_mv | 10.1074/jbc.M011000200 |
format | Article |
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We previously reported that all- trans -retinoic acid (t-RA) protected mesangial cells from H 2 O 2 -triggered apoptosis by suppressing the activator protein 1 (AP-1) pathway. It was via inhibition of c- fos and c- jun expression and suppression of c-Jun N-terminal kinase (JNK) activation. In this report, we investigated the involvement of
retinoic acid receptor (RAR) and retinoid X receptor (RXR) in the antiapoptotic effect of t-RA in H 2 O 2 -exposed cells. We found that pretreatment with RAR pan-antagonist (AGN193109) or RXR pan-antagonist (HX531) attenuated the
antiapoptotic effect of t-RA. Similarly, transient transfection with a dominant-negative mutant of RAR or a dominant-negative
RXR diminished the antiapoptotic effect of t-RA. Both RAR and RXR antagonists reversed the suppressive effect of t-RA on AP-1
activity. However, the roles of RAR and RXR in the suppression of AP-1 components by t-RA were found to be different. RAR
antagonist reversed the suppressive effect of t-RA on both c- fos and c- jun , whereas RXR antagonist reversed the effect of t-RA on c- fos but not c- jun . Furthermore, suppression of JNK activation by t-RA was observed even in the presence of RAR and RXR antagonists. Consistently,
suppression of JNK by t-RA was not affected by overexpression of either the dominant-negative RAR or the dominant-negative
RXR. These data elucidated that the antiapoptotic effect of t-RA is mediated by both nuclear receptor-dependent and -independent
mechanisms.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.M011000200</identifier><identifier>PMID: 11278809</identifier><language>eng</language><publisher>United States: American Society for Biochemistry and Molecular Biology</publisher><subject>Animals ; Apoptosis - drug effects ; Apoptosis - physiology ; c-fos gene ; c-jun gene ; Cells, Cultured ; Gene Expression Regulation - drug effects ; Genes, fos - drug effects ; Genes, jun - drug effects ; Glomerular Mesangium - cytology ; Glomerular Mesangium - drug effects ; Glomerular Mesangium - physiology ; Hydrogen Peroxide - pharmacology ; JNK Mitogen-Activated Protein Kinases ; JNK protein ; Male ; Mitogen-Activated Protein Kinases - metabolism ; Naphthalenes - pharmacology ; Phosphorylation ; Rats ; Rats, Sprague-Dawley ; Receptors, Retinoic Acid - antagonists & inhibitors ; Receptors, Retinoic Acid - drug effects ; Receptors, Retinoic Acid - physiology ; Recombinant Proteins - drug effects ; Recombinant Proteins - metabolism ; Retinoid X Receptors ; Transcription Factor AP-1 - metabolism ; Transcription Factors - drug effects ; Transcription Factors - physiology ; Transfection ; Tretinoin - pharmacology</subject><ispartof>The Journal of biological chemistry, 2001-04, Vol.276 (16), p.12697-12701</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c457t-a209d817937b1da6c318bda9654cab044ed8915aa59f85c8d750c119398c5fc43</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11278809$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Konta, T</creatorcontrib><creatorcontrib>Xu, Q</creatorcontrib><creatorcontrib>Furusu, A</creatorcontrib><creatorcontrib>Nakayama, K</creatorcontrib><creatorcontrib>Kitamura, M</creatorcontrib><title>Selective Roles of Retinoic Acid Receptor and Retinoid X Receptor in the Suppression of Apoptosis by All-trans-retinoic Acid</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>Retinoic acids exert profound effects on many biological processes including cell proliferation, differentiation, and morphogenesis.
We previously reported that all- trans -retinoic acid (t-RA) protected mesangial cells from H 2 O 2 -triggered apoptosis by suppressing the activator protein 1 (AP-1) pathway. It was via inhibition of c- fos and c- jun expression and suppression of c-Jun N-terminal kinase (JNK) activation. In this report, we investigated the involvement of
retinoic acid receptor (RAR) and retinoid X receptor (RXR) in the antiapoptotic effect of t-RA in H 2 O 2 -exposed cells. We found that pretreatment with RAR pan-antagonist (AGN193109) or RXR pan-antagonist (HX531) attenuated the
antiapoptotic effect of t-RA. Similarly, transient transfection with a dominant-negative mutant of RAR or a dominant-negative
RXR diminished the antiapoptotic effect of t-RA. Both RAR and RXR antagonists reversed the suppressive effect of t-RA on AP-1
activity. However, the roles of RAR and RXR in the suppression of AP-1 components by t-RA were found to be different. RAR
antagonist reversed the suppressive effect of t-RA on both c- fos and c- jun , whereas RXR antagonist reversed the effect of t-RA on c- fos but not c- jun . Furthermore, suppression of JNK activation by t-RA was observed even in the presence of RAR and RXR antagonists. Consistently,
suppression of JNK by t-RA was not affected by overexpression of either the dominant-negative RAR or the dominant-negative
RXR. These data elucidated that the antiapoptotic effect of t-RA is mediated by both nuclear receptor-dependent and -independent
mechanisms.</description><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - physiology</subject><subject>c-fos gene</subject><subject>c-jun gene</subject><subject>Cells, Cultured</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Genes, fos - drug effects</subject><subject>Genes, jun - drug effects</subject><subject>Glomerular Mesangium - cytology</subject><subject>Glomerular Mesangium - drug effects</subject><subject>Glomerular Mesangium - physiology</subject><subject>Hydrogen Peroxide - pharmacology</subject><subject>JNK Mitogen-Activated Protein Kinases</subject><subject>JNK protein</subject><subject>Male</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Naphthalenes - pharmacology</subject><subject>Phosphorylation</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Retinoic Acid - antagonists & inhibitors</subject><subject>Receptors, Retinoic Acid - drug effects</subject><subject>Receptors, Retinoic Acid - physiology</subject><subject>Recombinant Proteins - drug effects</subject><subject>Recombinant Proteins - metabolism</subject><subject>Retinoid X Receptors</subject><subject>Transcription Factor AP-1 - metabolism</subject><subject>Transcription Factors - drug effects</subject><subject>Transcription Factors - physiology</subject><subject>Transfection</subject><subject>Tretinoin - pharmacology</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkM1rGzEQxUVpaFyn1x6DDiW3dTW7K0s6mpAmBYdCPsA3oZVmY4X1aiutWwz54yNjFxcGhnnvN-_wCPkKbAZM1N9fGzu7ZwCMsZKxD2QCTFZFxWH1kUyyBoUquTwnn1N6zQyrFXwi5wClkJKpCXl7xA7t6P8gfQgdJhpa-oCj74O3dGG9y5fFYQyRmt79sxxdnXTf03GN9HE7DBFT8qHfhyyGkN3kE212dNF1xRhNn4r4f_YFOWtNl_DLcU_J84-bp-u7Yvnr9uf1YlnYmouxMCVTToJQlWjAmbmtQDbOqDmvrWlYXaOTCrgxXLWSW-kEZxZAVUpa3tq6mpKrQ-4Qw-8tplFvfLLYdabHsE0ahKxU5jM4O4A2hpQitnqIfmPiTgPT-7517luf-s4Pl8fkbbNBd8KPBWfg2wFY-5f1Xx9RNz7YNW50KeYa8pRzJap3G3KIFA</recordid><startdate>20010420</startdate><enddate>20010420</enddate><creator>Konta, T</creator><creator>Xu, Q</creator><creator>Furusu, A</creator><creator>Nakayama, K</creator><creator>Kitamura, M</creator><general>American Society for Biochemistry and Molecular Biology</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>7TM</scope></search><sort><creationdate>20010420</creationdate><title>Selective Roles of Retinoic Acid Receptor and Retinoid X Receptor in the Suppression of Apoptosis by All-trans-retinoic Acid</title><author>Konta, T ; Xu, Q ; Furusu, A ; Nakayama, K ; Kitamura, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c457t-a209d817937b1da6c318bda9654cab044ed8915aa59f85c8d750c119398c5fc43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - physiology</topic><topic>c-fos gene</topic><topic>c-jun gene</topic><topic>Cells, Cultured</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Genes, fos - drug effects</topic><topic>Genes, jun - drug effects</topic><topic>Glomerular Mesangium - cytology</topic><topic>Glomerular Mesangium - drug effects</topic><topic>Glomerular Mesangium - physiology</topic><topic>Hydrogen Peroxide - pharmacology</topic><topic>JNK Mitogen-Activated Protein Kinases</topic><topic>JNK protein</topic><topic>Male</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Naphthalenes - pharmacology</topic><topic>Phosphorylation</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Retinoic Acid - antagonists & inhibitors</topic><topic>Receptors, Retinoic Acid - drug effects</topic><topic>Receptors, Retinoic Acid - physiology</topic><topic>Recombinant Proteins - drug effects</topic><topic>Recombinant Proteins - metabolism</topic><topic>Retinoid X Receptors</topic><topic>Transcription Factor AP-1 - metabolism</topic><topic>Transcription Factors - drug effects</topic><topic>Transcription Factors - physiology</topic><topic>Transfection</topic><topic>Tretinoin - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Konta, T</creatorcontrib><creatorcontrib>Xu, Q</creatorcontrib><creatorcontrib>Furusu, A</creatorcontrib><creatorcontrib>Nakayama, K</creatorcontrib><creatorcontrib>Kitamura, M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><jtitle>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Konta, T</au><au>Xu, Q</au><au>Furusu, A</au><au>Nakayama, K</au><au>Kitamura, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Selective Roles of Retinoic Acid Receptor and Retinoid X Receptor in the Suppression of Apoptosis by All-trans-retinoic Acid</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>2001-04-20</date><risdate>2001</risdate><volume>276</volume><issue>16</issue><spage>12697</spage><epage>12701</epage><pages>12697-12701</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><abstract>Retinoic acids exert profound effects on many biological processes including cell proliferation, differentiation, and morphogenesis.
We previously reported that all- trans -retinoic acid (t-RA) protected mesangial cells from H 2 O 2 -triggered apoptosis by suppressing the activator protein 1 (AP-1) pathway. It was via inhibition of c- fos and c- jun expression and suppression of c-Jun N-terminal kinase (JNK) activation. In this report, we investigated the involvement of
retinoic acid receptor (RAR) and retinoid X receptor (RXR) in the antiapoptotic effect of t-RA in H 2 O 2 -exposed cells. We found that pretreatment with RAR pan-antagonist (AGN193109) or RXR pan-antagonist (HX531) attenuated the
antiapoptotic effect of t-RA. Similarly, transient transfection with a dominant-negative mutant of RAR or a dominant-negative
RXR diminished the antiapoptotic effect of t-RA. Both RAR and RXR antagonists reversed the suppressive effect of t-RA on AP-1
activity. However, the roles of RAR and RXR in the suppression of AP-1 components by t-RA were found to be different. RAR
antagonist reversed the suppressive effect of t-RA on both c- fos and c- jun , whereas RXR antagonist reversed the effect of t-RA on c- fos but not c- jun . Furthermore, suppression of JNK activation by t-RA was observed even in the presence of RAR and RXR antagonists. Consistently,
suppression of JNK by t-RA was not affected by overexpression of either the dominant-negative RAR or the dominant-negative
RXR. These data elucidated that the antiapoptotic effect of t-RA is mediated by both nuclear receptor-dependent and -independent
mechanisms.</abstract><cop>United States</cop><pub>American Society for Biochemistry and Molecular Biology</pub><pmid>11278809</pmid><doi>10.1074/jbc.M011000200</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Apoptosis - drug effects Apoptosis - physiology c-fos gene c-jun gene Cells, Cultured Gene Expression Regulation - drug effects Genes, fos - drug effects Genes, jun - drug effects Glomerular Mesangium - cytology Glomerular Mesangium - drug effects Glomerular Mesangium - physiology Hydrogen Peroxide - pharmacology JNK Mitogen-Activated Protein Kinases JNK protein Male Mitogen-Activated Protein Kinases - metabolism Naphthalenes - pharmacology Phosphorylation Rats Rats, Sprague-Dawley Receptors, Retinoic Acid - antagonists & inhibitors Receptors, Retinoic Acid - drug effects Receptors, Retinoic Acid - physiology Recombinant Proteins - drug effects Recombinant Proteins - metabolism Retinoid X Receptors Transcription Factor AP-1 - metabolism Transcription Factors - drug effects Transcription Factors - physiology Transfection Tretinoin - pharmacology |
title | Selective Roles of Retinoic Acid Receptor and Retinoid X Receptor in the Suppression of Apoptosis by All-trans-retinoic Acid |
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