Estradiol induction of rhodamine 123 efflux and the multidrug resistance pump in rat pituitary tumor cells
Rhodamine 123 is a fluorescent dye that localizes in mitochondria, is a substrate for the multidrug resistance pump, and is retained for long periods of time by carcinoma cells. 17 beta-Estradiol causes GH4C1 cells (rat pituitary tumor cells) to lose rhodamine 123 fluorescence faster than untreated...
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| Veröffentlicht in: | Molecular pharmacology 1993-01, Vol.43 (1), p.51-56 |
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| container_title | Molecular pharmacology |
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| creator | JANCIS, E. M CARBONE, R LOECHNER, K. J DANNIES, P. S |
| description | Rhodamine 123 is a fluorescent dye that localizes in mitochondria, is a substrate for the multidrug resistance pump, and is
retained for long periods of time by carcinoma cells. 17 beta-Estradiol causes GH4C1 cells (rat pituitary tumor cells) to
lose rhodamine 123 fluorescence faster than untreated cells. We found that estradiol induces accumulation of the mRNA for
the multidrug resistance pump 3-5-fold, with maximum induction occurring within 1 day at 10(-9) M estradiol. Immunoblot analysis
demonstrated that estradiol induces a protein of 150 kDa that reacts with an antibody to P-glycoprotein, the multidrug resistance
pump. The reduced retention of rhodamine 123 caused by estradiol is prevented by verapamil and cyclosporin, inhibitors of
the pump. A clone resistant to the effects of estradiol on rhodamine 123 has greatly reduced levels of mRNA for the pump.
The effect of estradiol is more marked on rhodamine 123 retention than it is on that of rhodamine 110 or tetramethylrhodamine
methyl ester. We conclude that estradiol enhances rhodamine 123 efflux by inducing the multidrug resistance gene. The specificity
for rhodamine 123, compared with other analogs, may be caused by differences in accessibility to the pump. |
| format | Article |
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retained for long periods of time by carcinoma cells. 17 beta-Estradiol causes GH4C1 cells (rat pituitary tumor cells) to
lose rhodamine 123 fluorescence faster than untreated cells. We found that estradiol induces accumulation of the mRNA for
the multidrug resistance pump 3-5-fold, with maximum induction occurring within 1 day at 10(-9) M estradiol. Immunoblot analysis
demonstrated that estradiol induces a protein of 150 kDa that reacts with an antibody to P-glycoprotein, the multidrug resistance
pump. The reduced retention of rhodamine 123 caused by estradiol is prevented by verapamil and cyclosporin, inhibitors of
the pump. A clone resistant to the effects of estradiol on rhodamine 123 has greatly reduced levels of mRNA for the pump.
The effect of estradiol is more marked on rhodamine 123 retention than it is on that of rhodamine 110 or tetramethylrhodamine
methyl ester. We conclude that estradiol enhances rhodamine 123 efflux by inducing the multidrug resistance gene. The specificity
for rhodamine 123, compared with other analogs, may be caused by differences in accessibility to the pump.</description><identifier>ISSN: 0026-895X</identifier><identifier>EISSN: 1521-0111</identifier><identifier>PMID: 8423769</identifier><identifier>CODEN: MOPMA3</identifier><language>eng</language><publisher>Bethesda, MD: American Society for Pharmacology and Experimental Therapeutics</publisher><subject>Animals ; Antineoplastic agents ; Biological and medical sciences ; Cyclosporins - pharmacology ; Drug Resistance - genetics ; Estradiol - pharmacology ; General aspects ; Medical sciences ; Pharmacology. Drug treatments ; Pituitary Neoplasms - metabolism ; Rats ; Rhodamine 123 ; Rhodamines - pharmacokinetics ; RNA, Messenger - analysis ; Tumor Cells, Cultured ; Verapamil - pharmacology</subject><ispartof>Molecular pharmacology, 1993-01, Vol.43 (1), p.51-56</ispartof><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,4022</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4569448$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8423769$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>JANCIS, E. M</creatorcontrib><creatorcontrib>CARBONE, R</creatorcontrib><creatorcontrib>LOECHNER, K. J</creatorcontrib><creatorcontrib>DANNIES, P. S</creatorcontrib><title>Estradiol induction of rhodamine 123 efflux and the multidrug resistance pump in rat pituitary tumor cells</title><title>Molecular pharmacology</title><addtitle>Mol Pharmacol</addtitle><description>Rhodamine 123 is a fluorescent dye that localizes in mitochondria, is a substrate for the multidrug resistance pump, and is
retained for long periods of time by carcinoma cells. 17 beta-Estradiol causes GH4C1 cells (rat pituitary tumor cells) to
lose rhodamine 123 fluorescence faster than untreated cells. We found that estradiol induces accumulation of the mRNA for
the multidrug resistance pump 3-5-fold, with maximum induction occurring within 1 day at 10(-9) M estradiol. Immunoblot analysis
demonstrated that estradiol induces a protein of 150 kDa that reacts with an antibody to P-glycoprotein, the multidrug resistance
pump. The reduced retention of rhodamine 123 caused by estradiol is prevented by verapamil and cyclosporin, inhibitors of
the pump. A clone resistant to the effects of estradiol on rhodamine 123 has greatly reduced levels of mRNA for the pump.
The effect of estradiol is more marked on rhodamine 123 retention than it is on that of rhodamine 110 or tetramethylrhodamine
methyl ester. We conclude that estradiol enhances rhodamine 123 efflux by inducing the multidrug resistance gene. The specificity
for rhodamine 123, compared with other analogs, may be caused by differences in accessibility to the pump.</description><subject>Animals</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Cyclosporins - pharmacology</subject><subject>Drug Resistance - genetics</subject><subject>Estradiol - pharmacology</subject><subject>General aspects</subject><subject>Medical sciences</subject><subject>Pharmacology. Drug treatments</subject><subject>Pituitary Neoplasms - metabolism</subject><subject>Rats</subject><subject>Rhodamine 123</subject><subject>Rhodamines - pharmacokinetics</subject><subject>RNA, Messenger - analysis</subject><subject>Tumor Cells, Cultured</subject><subject>Verapamil - pharmacology</subject><issn>0026-895X</issn><issn>1521-0111</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEtLxDAAhIso67r6E4QcxFshj6ZJjrKsDxC8KHgraR7bLG1T80D991YsevQ0h_kYZuaoWCOKUQkRQsfFGkJcl1zQ19PiLMYDhKiiHK6KFa8wYbVYF4ddTEFq53vgRp1Vcn4E3oLQeS0HNxqAMAHG2j5_ADlqkDoDhtwnp0Peg2Cii0mOyoApD9OcAYJMYHIpuyTDJ0h58AEo0_fxvDixso_mYtFN8XK7e97el49Pdw_bm8eyw4Km0piaIa604ratdS21gFoai7DginNrlYCVrpAUlZUtwQRh3DKmGRF2rokZ2RTXP7lT8G_ZxNQMLn43kKPxOTaMUgZ5Df8FUU0JYpjM4OUC5nYwupmCG-ZxzfLi7F8tvoxK9jbMh7j4i1W0FlXF_7DO7bt3F0wzdTIMUvne72eMNKihiHwBoYuKgg</recordid><startdate>19930101</startdate><enddate>19930101</enddate><creator>JANCIS, E. M</creator><creator>CARBONE, R</creator><creator>LOECHNER, K. J</creator><creator>DANNIES, P. S</creator><general>American Society for Pharmacology and Experimental Therapeutics</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>19930101</creationdate><title>Estradiol induction of rhodamine 123 efflux and the multidrug resistance pump in rat pituitary tumor cells</title><author>JANCIS, E. M ; CARBONE, R ; LOECHNER, K. J ; DANNIES, P. S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h295t-ee6718cdc8fb6d6ad90daef1298c88ffc904d41a94fab323122b77d739feff273</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Animals</topic><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>Cyclosporins - pharmacology</topic><topic>Drug Resistance - genetics</topic><topic>Estradiol - pharmacology</topic><topic>General aspects</topic><topic>Medical sciences</topic><topic>Pharmacology. Drug treatments</topic><topic>Pituitary Neoplasms - metabolism</topic><topic>Rats</topic><topic>Rhodamine 123</topic><topic>Rhodamines - pharmacokinetics</topic><topic>RNA, Messenger - analysis</topic><topic>Tumor Cells, Cultured</topic><topic>Verapamil - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>JANCIS, E. M</creatorcontrib><creatorcontrib>CARBONE, R</creatorcontrib><creatorcontrib>LOECHNER, K. J</creatorcontrib><creatorcontrib>DANNIES, P. S</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>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>JANCIS, E. M</au><au>CARBONE, R</au><au>LOECHNER, K. J</au><au>DANNIES, P. S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Estradiol induction of rhodamine 123 efflux and the multidrug resistance pump in rat pituitary tumor cells</atitle><jtitle>Molecular pharmacology</jtitle><addtitle>Mol Pharmacol</addtitle><date>1993-01-01</date><risdate>1993</risdate><volume>43</volume><issue>1</issue><spage>51</spage><epage>56</epage><pages>51-56</pages><issn>0026-895X</issn><eissn>1521-0111</eissn><coden>MOPMA3</coden><abstract>Rhodamine 123 is a fluorescent dye that localizes in mitochondria, is a substrate for the multidrug resistance pump, and is
retained for long periods of time by carcinoma cells. 17 beta-Estradiol causes GH4C1 cells (rat pituitary tumor cells) to
lose rhodamine 123 fluorescence faster than untreated cells. We found that estradiol induces accumulation of the mRNA for
the multidrug resistance pump 3-5-fold, with maximum induction occurring within 1 day at 10(-9) M estradiol. Immunoblot analysis
demonstrated that estradiol induces a protein of 150 kDa that reacts with an antibody to P-glycoprotein, the multidrug resistance
pump. The reduced retention of rhodamine 123 caused by estradiol is prevented by verapamil and cyclosporin, inhibitors of
the pump. A clone resistant to the effects of estradiol on rhodamine 123 has greatly reduced levels of mRNA for the pump.
The effect of estradiol is more marked on rhodamine 123 retention than it is on that of rhodamine 110 or tetramethylrhodamine
methyl ester. We conclude that estradiol enhances rhodamine 123 efflux by inducing the multidrug resistance gene. The specificity
for rhodamine 123, compared with other analogs, may be caused by differences in accessibility to the pump.</abstract><cop>Bethesda, MD</cop><pub>American Society for Pharmacology and Experimental Therapeutics</pub><pmid>8423769</pmid><tpages>6</tpages></addata></record> |
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| ispartof | Molecular pharmacology, 1993-01, Vol.43 (1), p.51-56 |
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| language | eng |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Antineoplastic agents Biological and medical sciences Cyclosporins - pharmacology Drug Resistance - genetics Estradiol - pharmacology General aspects Medical sciences Pharmacology. Drug treatments Pituitary Neoplasms - metabolism Rats Rhodamine 123 Rhodamines - pharmacokinetics RNA, Messenger - analysis Tumor Cells, Cultured Verapamil - pharmacology |
| title | Estradiol induction of rhodamine 123 efflux and the multidrug resistance pump in rat pituitary tumor cells |
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