Modulation of CCK mRNA in cell lines in response to isoproterenol and retinoic acid
Regulation of cholecystokinin (CCK) expression was studied in the human neuroepithelioma cell line SK-N-MCIXC and the rat medullary thyroid carcinoma cell line WE 4/2. The cells were treated with the β-adrenergic agonist isoproterenol and retinoic acid, a natural derivative of vitamin A, which plays...
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| Veröffentlicht in: | Neuropeptides (Edinburgh) 1995-10, Vol.29 (4), p.221-227 |
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| creator | Mania-Farnell, B.L Botros, I.W Davis, T.P |
| description | Regulation of cholecystokinin (CCK) expression was studied in the human neuroepithelioma cell line SK-N-MCIXC and the rat medullary thyroid carcinoma cell line WE 4/2. The cells were treated with the β-adrenergic agonist isoproterenol and retinoic acid, a natural derivative of vitamin A, which plays a role in cell growth and proliferation. Levels of CCK mRNA were determined after 6, 12 and 24 h drug treatments, with Northern blot analysis using human CCK riboprobes. In WE 4/2 cells no differences were observed in CCK mRNA levels, between control and isoproterenol treated cells, after 6, 12 or 24 h treatments. In SK-N-MCIXC cells isoproterenol increased CCK mRNA levels at all time points examined, the β-adrenergic antagonist propranolol blocked this effect. SK-N-MCIXC cells were also treated with actinomycin D or cycloheximide in combination with isoproterenol. Actinomycin D decreased CCK mRNA levels. Cycloheximide increased CCK mRNA levels when compared to isoproterenol acting alone. Retinoic acid did not affect CCK mRNA levels in WE 4/2 cells. In SK-N-MCIXC cells, retinoic acid consistently decreased CCK mRNA level. CCK mRNA levels in SK-N-MCIXC cells treated with retinoic acid combined with either isoproterenol or phorbol-12-myristate-13 acetate, were not significantly different from cells treated with retinoic acid alone. |
| doi_str_mv | 10.1016/0143-4179(95)90064-0 |
| format | Article |
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The cells were treated with the β-adrenergic agonist isoproterenol and retinoic acid, a natural derivative of vitamin A, which plays a role in cell growth and proliferation. Levels of CCK mRNA were determined after 6, 12 and 24 h drug treatments, with Northern blot analysis using human CCK riboprobes. In WE 4/2 cells no differences were observed in CCK mRNA levels, between control and isoproterenol treated cells, after 6, 12 or 24 h treatments. In SK-N-MCIXC cells isoproterenol increased CCK mRNA levels at all time points examined, the β-adrenergic antagonist propranolol blocked this effect. SK-N-MCIXC cells were also treated with actinomycin D or cycloheximide in combination with isoproterenol. Actinomycin D decreased CCK mRNA levels. Cycloheximide increased CCK mRNA levels when compared to isoproterenol acting alone. Retinoic acid did not affect CCK mRNA levels in WE 4/2 cells. In SK-N-MCIXC cells, retinoic acid consistently decreased CCK mRNA level. CCK mRNA levels in SK-N-MCIXC cells treated with retinoic acid combined with either isoproterenol or phorbol-12-myristate-13 acetate, were not significantly different from cells treated with retinoic acid alone.</description><identifier>ISSN: 0143-4179</identifier><identifier>EISSN: 1532-2785</identifier><identifier>DOI: 10.1016/0143-4179(95)90064-0</identifier><identifier>PMID: 8584140</identifier><identifier>CODEN: NRPPDD</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Adrenergic beta-Agonists - pharmacology ; Animals ; Autoradiography ; Biological and medical sciences ; Blotting, Northern ; Cholecystokinin - biosynthesis ; Cholecystokinin - genetics ; Fundamental and applied biological sciences. Psychology ; Gene expression ; Gene Expression - drug effects ; Humans ; In Situ Hybridization ; Isoproterenol - pharmacology ; Keratolytic Agents - pharmacology ; Molecular and cellular biology ; Molecular genetics ; Rats ; RNA Probes ; RNA, Messenger - biosynthesis ; Tretinoin - pharmacology ; Tumor Cells, Cultured</subject><ispartof>Neuropeptides (Edinburgh), 1995-10, Vol.29 (4), p.221-227</ispartof><rights>1995</rights><rights>1995 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c332t-49414027dd9a5bd16643ecce32bf28b15710c83f021a4ec4dc67b06a8c96e8cb3</citedby><cites>FETCH-LOGICAL-c332t-49414027dd9a5bd16643ecce32bf28b15710c83f021a4ec4dc67b06a8c96e8cb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0143-4179(95)90064-0$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3693592$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8584140$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mania-Farnell, B.L</creatorcontrib><creatorcontrib>Botros, I.W</creatorcontrib><creatorcontrib>Davis, T.P</creatorcontrib><title>Modulation of CCK mRNA in cell lines in response to isoproterenol and retinoic acid</title><title>Neuropeptides (Edinburgh)</title><addtitle>Neuropeptides</addtitle><description>Regulation of cholecystokinin (CCK) expression was studied in the human neuroepithelioma cell line SK-N-MCIXC and the rat medullary thyroid carcinoma cell line WE 4/2. The cells were treated with the β-adrenergic agonist isoproterenol and retinoic acid, a natural derivative of vitamin A, which plays a role in cell growth and proliferation. Levels of CCK mRNA were determined after 6, 12 and 24 h drug treatments, with Northern blot analysis using human CCK riboprobes. In WE 4/2 cells no differences were observed in CCK mRNA levels, between control and isoproterenol treated cells, after 6, 12 or 24 h treatments. In SK-N-MCIXC cells isoproterenol increased CCK mRNA levels at all time points examined, the β-adrenergic antagonist propranolol blocked this effect. SK-N-MCIXC cells were also treated with actinomycin D or cycloheximide in combination with isoproterenol. Actinomycin D decreased CCK mRNA levels. Cycloheximide increased CCK mRNA levels when compared to isoproterenol acting alone. Retinoic acid did not affect CCK mRNA levels in WE 4/2 cells. In SK-N-MCIXC cells, retinoic acid consistently decreased CCK mRNA level. CCK mRNA levels in SK-N-MCIXC cells treated with retinoic acid combined with either isoproterenol or phorbol-12-myristate-13 acetate, were not significantly different from cells treated with retinoic acid alone.</description><subject>Adrenergic beta-Agonists - pharmacology</subject><subject>Animals</subject><subject>Autoradiography</subject><subject>Biological and medical sciences</subject><subject>Blotting, Northern</subject><subject>Cholecystokinin - biosynthesis</subject><subject>Cholecystokinin - genetics</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene expression</subject><subject>Gene Expression - drug effects</subject><subject>Humans</subject><subject>In Situ Hybridization</subject><subject>Isoproterenol - pharmacology</subject><subject>Keratolytic Agents - pharmacology</subject><subject>Molecular and cellular biology</subject><subject>Molecular genetics</subject><subject>Rats</subject><subject>RNA Probes</subject><subject>RNA, Messenger - biosynthesis</subject><subject>Tretinoin - pharmacology</subject><subject>Tumor Cells, Cultured</subject><issn>0143-4179</issn><issn>1532-2785</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkF1rFDEUhoMo7bb6DxRyIUUvRvM1meSmUBarYmuh6nXInJyBlNlkTWYL_ffOuMteam4O4X3O4eUh5DVnHzjj-iPjSjaKd_adbd9bxrRq2DOy4q0UjehM-5ysjsgpOav1gTGmhDEn5MS0RnHFVuTHbQ670U8xJ5oHul5_o5v771c0Jgo4jnSMCevyK1i3OVWkU6ax5m3JExZMeaQ-hTmdYsoRqIcYXpIXgx8rvjrMc_Lr-tPP9Zfm5u7z1_XVTQNSiqlRdqkguhCsb_vAtVYSAVCKfhCm523HGRg5MMG9QlABdNcz7Q1YjQZ6eU4u9nfnMr93WCe3iXVp7RPmXXXd_KzR4r8g19Zwa80Mqj0IJddacHDbEje-PDnO3CLdLUbdYtTZ1v2V7ti89uZwf9dvMByXDpbn_O0h9xX8OBSfINYjJrWVrV1qXu4xnKU9RiyuQsQEGGJBmFzI8d89_gBjtZxR</recordid><startdate>199510</startdate><enddate>199510</enddate><creator>Mania-Farnell, B.L</creator><creator>Botros, I.W</creator><creator>Davis, T.P</creator><general>Elsevier Ltd</general><general>Elsevier</general><scope>IQODW</scope><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>7TK</scope><scope>7X8</scope></search><sort><creationdate>199510</creationdate><title>Modulation of CCK mRNA in cell lines in response to isoproterenol and retinoic acid</title><author>Mania-Farnell, B.L ; Botros, I.W ; Davis, T.P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c332t-49414027dd9a5bd16643ecce32bf28b15710c83f021a4ec4dc67b06a8c96e8cb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Adrenergic beta-Agonists - pharmacology</topic><topic>Animals</topic><topic>Autoradiography</topic><topic>Biological and medical sciences</topic><topic>Blotting, Northern</topic><topic>Cholecystokinin - biosynthesis</topic><topic>Cholecystokinin - genetics</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene expression</topic><topic>Gene Expression - drug effects</topic><topic>Humans</topic><topic>In Situ Hybridization</topic><topic>Isoproterenol - pharmacology</topic><topic>Keratolytic Agents - pharmacology</topic><topic>Molecular and cellular biology</topic><topic>Molecular genetics</topic><topic>Rats</topic><topic>RNA Probes</topic><topic>RNA, Messenger - biosynthesis</topic><topic>Tretinoin - pharmacology</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mania-Farnell, B.L</creatorcontrib><creatorcontrib>Botros, I.W</creatorcontrib><creatorcontrib>Davis, T.P</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>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neuropeptides (Edinburgh)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mania-Farnell, B.L</au><au>Botros, I.W</au><au>Davis, T.P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Modulation of CCK mRNA in cell lines in response to isoproterenol and retinoic acid</atitle><jtitle>Neuropeptides (Edinburgh)</jtitle><addtitle>Neuropeptides</addtitle><date>1995-10</date><risdate>1995</risdate><volume>29</volume><issue>4</issue><spage>221</spage><epage>227</epage><pages>221-227</pages><issn>0143-4179</issn><eissn>1532-2785</eissn><coden>NRPPDD</coden><abstract>Regulation of cholecystokinin (CCK) expression was studied in the human neuroepithelioma cell line SK-N-MCIXC and the rat medullary thyroid carcinoma cell line WE 4/2. The cells were treated with the β-adrenergic agonist isoproterenol and retinoic acid, a natural derivative of vitamin A, which plays a role in cell growth and proliferation. Levels of CCK mRNA were determined after 6, 12 and 24 h drug treatments, with Northern blot analysis using human CCK riboprobes. In WE 4/2 cells no differences were observed in CCK mRNA levels, between control and isoproterenol treated cells, after 6, 12 or 24 h treatments. In SK-N-MCIXC cells isoproterenol increased CCK mRNA levels at all time points examined, the β-adrenergic antagonist propranolol blocked this effect. SK-N-MCIXC cells were also treated with actinomycin D or cycloheximide in combination with isoproterenol. Actinomycin D decreased CCK mRNA levels. Cycloheximide increased CCK mRNA levels when compared to isoproterenol acting alone. Retinoic acid did not affect CCK mRNA levels in WE 4/2 cells. In SK-N-MCIXC cells, retinoic acid consistently decreased CCK mRNA level. CCK mRNA levels in SK-N-MCIXC cells treated with retinoic acid combined with either isoproterenol or phorbol-12-myristate-13 acetate, were not significantly different from cells treated with retinoic acid alone.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>8584140</pmid><doi>10.1016/0143-4179(95)90064-0</doi><tpages>7</tpages></addata></record> |
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| subjects | Adrenergic beta-Agonists - pharmacology Animals Autoradiography Biological and medical sciences Blotting, Northern Cholecystokinin - biosynthesis Cholecystokinin - genetics Fundamental and applied biological sciences. Psychology Gene expression Gene Expression - drug effects Humans In Situ Hybridization Isoproterenol - pharmacology Keratolytic Agents - pharmacology Molecular and cellular biology Molecular genetics Rats RNA Probes RNA, Messenger - biosynthesis Tretinoin - pharmacology Tumor Cells, Cultured |
| title | Modulation of CCK mRNA in cell lines in response to isoproterenol and retinoic acid |
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