RGS2 Is Regulated by Angiotensin II and Functions as a Negative Feedback of Aldosterone Production in H295R Human Adrenocortical Cells
Regulator of G protein signaling (RGS) proteins interact with Gα-subunits of heterotrimeric G proteins, accelerating the rate of GTP hydrolysis and finalizing the intracellular signaling triggered by the G protein-coupled receptor-ligand interaction. Angiotensin (Ang) II interacts with its G protein...
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| Veröffentlicht in: | Endocrinology (Philadelphia) 2006-08, Vol.147 (8), p.3889-3897 |
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| creator | Romero, Damian G Plonczynski, Maria W Gomez-Sanchez, Elise P Yanes, Licy L Gomez-Sanchez, Celso E |
| description | Regulator of G protein signaling (RGS) proteins interact with Gα-subunits of heterotrimeric G proteins, accelerating the rate of GTP hydrolysis and finalizing the intracellular signaling triggered by the G protein-coupled receptor-ligand interaction. Angiotensin (Ang) II interacts with its G protein-coupled receptor in zona glomerulosa adrenal cells and triggers a cascade of intracellular signals that regulates steroidogenesis and proliferation. We studied Ang II-mediated regulation of RGS2, the role of RGS2 in steroidogenesis, and the intracellular signal events involved in H295R human adrenal cells. We report that both H295R cells and human adrenal gland express RGS2 mRNA. In H295R cells, Ang II caused a rapid and transient increase in RGS2 mRNA levels quantified by real-time RT-PCR. Ang II effects were mimicked by calcium ionophore A23187 and blocked by calcium channel blocker nifedipine. Ang II effects also were blocked by calmodulin antagonists (W-7 and calmidazolium) and calcium/calmodulin-dependent kinase antagonist KN-93. RGS2 overexpression by retroviral infection in H295R cells caused a decrease in Ang II-stimulated aldosterone secretion but did not modify cortisol secretion. In reporter assays, RGS2 decreased Ang II-mediated aldosterone synthase up-regulation. These results suggest that Ang II up-regulates RGS2 mRNA by the calcium/calmodulin-dependent kinase pathway in H295R cells. RGS2 overexpression specifically decreases aldosterone secretion through a decrease in Ang II-mediated aldosterone synthase-induced expression. In conclusion, RGS2 expression is induced by Ang II to terminate the intracellular signaling cascade generated by Ang II. RGS2 alterations in expression levels or functionality could be implicated in deregulations of Ang II signaling and abnormal aldosterone secretion by the adrenal gland. |
| doi_str_mv | 10.1210/en.2005-1532 |
| format | Article |
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Angiotensin (Ang) II interacts with its G protein-coupled receptor in zona glomerulosa adrenal cells and triggers a cascade of intracellular signals that regulates steroidogenesis and proliferation. We studied Ang II-mediated regulation of RGS2, the role of RGS2 in steroidogenesis, and the intracellular signal events involved in H295R human adrenal cells. We report that both H295R cells and human adrenal gland express RGS2 mRNA. In H295R cells, Ang II caused a rapid and transient increase in RGS2 mRNA levels quantified by real-time RT-PCR. Ang II effects were mimicked by calcium ionophore A23187 and blocked by calcium channel blocker nifedipine. Ang II effects also were blocked by calmodulin antagonists (W-7 and calmidazolium) and calcium/calmodulin-dependent kinase antagonist KN-93. RGS2 overexpression by retroviral infection in H295R cells caused a decrease in Ang II-stimulated aldosterone secretion but did not modify cortisol secretion. In reporter assays, RGS2 decreased Ang II-mediated aldosterone synthase up-regulation. These results suggest that Ang II up-regulates RGS2 mRNA by the calcium/calmodulin-dependent kinase pathway in H295R cells. RGS2 overexpression specifically decreases aldosterone secretion through a decrease in Ang II-mediated aldosterone synthase-induced expression. In conclusion, RGS2 expression is induced by Ang II to terminate the intracellular signaling cascade generated by Ang II. RGS2 alterations in expression levels or functionality could be implicated in deregulations of Ang II signaling and abnormal aldosterone secretion by the adrenal gland.</description><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/en.2005-1532</identifier><identifier>PMID: 16627589</identifier><identifier>CODEN: ENDOAO</identifier><language>eng</language><publisher>Bethesda, MD: Endocrine Society</publisher><subject>Adrenal Cortex - cytology ; Adrenal Cortex - metabolism ; Adrenal Cortex - secretion ; Adrenal glands ; Aldosterone ; Aldosterone - biosynthesis ; Aldosterone - metabolism ; Aldosterone - secretion ; Aldosterone synthase ; Angiotensin ; Angiotensin II ; Angiotensin II - metabolism ; Angiotensin II - pharmacology ; Antagonists ; Biological and medical sciences ; Calcimycin ; Calcium antagonists ; Calcium channel blockers ; Calcium channels ; Calcium ionophores ; Calcium Signaling - drug effects ; Calcium Signaling - physiology ; Calcium-Calmodulin-Dependent Protein Kinases - metabolism ; Calmodulin ; Calmodulin - metabolism ; Cell Line ; Cell proliferation ; Cytochrome P-450 CYP11B2 - metabolism ; Deregulation ; Feedback, Physiological - physiology ; Fundamental and applied biological sciences. Psychology ; Gene Expression - drug effects ; Gene Expression - physiology ; Humans ; Intracellular ; Intracellular signalling ; Kinases ; mRNA ; Negative feedback ; Nifedipine ; Protein Kinase C - metabolism ; Proteins ; Real time ; Receptors ; RGS Proteins - genetics ; RGS Proteins - metabolism ; RNA, Messenger - metabolism ; Secretion ; Steroid 11-beta-Hydroxylase - metabolism ; Steroidogenesis ; Up-Regulation - drug effects ; Up-Regulation - physiology ; Vasoconstrictor Agents - metabolism ; Vasoconstrictor Agents - pharmacology ; Vertebrates: endocrinology</subject><ispartof>Endocrinology (Philadelphia), 2006-08, Vol.147 (8), p.3889-3897</ispartof><rights>Copyright © 2006 by The Endocrine Society 2006</rights><rights>2006 INIST-CNRS</rights><rights>Copyright © 2006 by The Endocrine Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c558t-c1ce2b9bb86370987823287fe1c924c32fa79152ef4b6dfd16f54cd9978d4463</citedby><cites>FETCH-LOGICAL-c558t-c1ce2b9bb86370987823287fe1c924c32fa79152ef4b6dfd16f54cd9978d4463</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17957267$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16627589$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Romero, Damian G</creatorcontrib><creatorcontrib>Plonczynski, Maria W</creatorcontrib><creatorcontrib>Gomez-Sanchez, Elise P</creatorcontrib><creatorcontrib>Yanes, Licy L</creatorcontrib><creatorcontrib>Gomez-Sanchez, Celso E</creatorcontrib><title>RGS2 Is Regulated by Angiotensin II and Functions as a Negative Feedback of Aldosterone Production in H295R Human Adrenocortical Cells</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>Regulator of G protein signaling (RGS) proteins interact with Gα-subunits of heterotrimeric G proteins, accelerating the rate of GTP hydrolysis and finalizing the intracellular signaling triggered by the G protein-coupled receptor-ligand interaction. Angiotensin (Ang) II interacts with its G protein-coupled receptor in zona glomerulosa adrenal cells and triggers a cascade of intracellular signals that regulates steroidogenesis and proliferation. We studied Ang II-mediated regulation of RGS2, the role of RGS2 in steroidogenesis, and the intracellular signal events involved in H295R human adrenal cells. We report that both H295R cells and human adrenal gland express RGS2 mRNA. In H295R cells, Ang II caused a rapid and transient increase in RGS2 mRNA levels quantified by real-time RT-PCR. Ang II effects were mimicked by calcium ionophore A23187 and blocked by calcium channel blocker nifedipine. Ang II effects also were blocked by calmodulin antagonists (W-7 and calmidazolium) and calcium/calmodulin-dependent kinase antagonist KN-93. RGS2 overexpression by retroviral infection in H295R cells caused a decrease in Ang II-stimulated aldosterone secretion but did not modify cortisol secretion. In reporter assays, RGS2 decreased Ang II-mediated aldosterone synthase up-regulation. These results suggest that Ang II up-regulates RGS2 mRNA by the calcium/calmodulin-dependent kinase pathway in H295R cells. RGS2 overexpression specifically decreases aldosterone secretion through a decrease in Ang II-mediated aldosterone synthase-induced expression. In conclusion, RGS2 expression is induced by Ang II to terminate the intracellular signaling cascade generated by Ang II. RGS2 alterations in expression levels or functionality could be implicated in deregulations of Ang II signaling and abnormal aldosterone secretion by the adrenal gland.</description><subject>Adrenal Cortex - cytology</subject><subject>Adrenal Cortex - metabolism</subject><subject>Adrenal Cortex - secretion</subject><subject>Adrenal glands</subject><subject>Aldosterone</subject><subject>Aldosterone - biosynthesis</subject><subject>Aldosterone - metabolism</subject><subject>Aldosterone - secretion</subject><subject>Aldosterone synthase</subject><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Angiotensin II - metabolism</subject><subject>Angiotensin II - pharmacology</subject><subject>Antagonists</subject><subject>Biological and medical sciences</subject><subject>Calcimycin</subject><subject>Calcium antagonists</subject><subject>Calcium channel blockers</subject><subject>Calcium channels</subject><subject>Calcium ionophores</subject><subject>Calcium Signaling - drug effects</subject><subject>Calcium Signaling - physiology</subject><subject>Calcium-Calmodulin-Dependent Protein Kinases - metabolism</subject><subject>Calmodulin</subject><subject>Calmodulin - metabolism</subject><subject>Cell Line</subject><subject>Cell proliferation</subject><subject>Cytochrome P-450 CYP11B2 - metabolism</subject><subject>Deregulation</subject><subject>Feedback, Physiological - physiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression - drug effects</subject><subject>Gene Expression - physiology</subject><subject>Humans</subject><subject>Intracellular</subject><subject>Intracellular signalling</subject><subject>Kinases</subject><subject>mRNA</subject><subject>Negative feedback</subject><subject>Nifedipine</subject><subject>Protein Kinase C - metabolism</subject><subject>Proteins</subject><subject>Real time</subject><subject>Receptors</subject><subject>RGS Proteins - genetics</subject><subject>RGS Proteins - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>Secretion</subject><subject>Steroid 11-beta-Hydroxylase - metabolism</subject><subject>Steroidogenesis</subject><subject>Up-Regulation - drug effects</subject><subject>Up-Regulation - physiology</subject><subject>Vasoconstrictor Agents - metabolism</subject><subject>Vasoconstrictor Agents - pharmacology</subject><subject>Vertebrates: endocrinology</subject><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10V1r2zAUBmAxVtas292uh2B0vak7fVrWZQhLEyjdyHpvZOk4uHOkTLIH_QP73VMaQ2CsIBCCR-cc6UXoAyU3lFHyBfwNI0QWVHL2Cs2oFrJQVJHXaEYI5YViTJ2jtyk95qMQgr9B57QsmZKVnqE_m9sfDK8T3sB27M0ADjdPeO63XRjAp87j9Rob7_By9Hbogk_Y5IXvYWuG7jfgJYBrjP2JQ4vnvQtpgBg84O8xuPH5Bs5FVkzLDV6NO-Px3EXwwYY4dNb0eAF9n96hs9b0Cd5P-wV6WH59WKyKu2-368X8rrBSVkNhqQXW6KapSq6IrlTFOKtUC9RqJixnrVGaSgataErXOlq2UlintaqcECW_QJ-PZfcx_BohDfWuSzYPYDyEMdU0S0JLmuGnf-BjGKPPo9WcciLLSqgqq-ujsjGkFKGt97HbmfhUU1IfwqnB14dw6kM4mX-cio7NDtwJT2lkcDkBk_LXtNF426WTU1oqVqrsro4ujPuXWhZTS36U4F2wsfOwj5DS6TX_HfQvkS6yaw</recordid><startdate>20060801</startdate><enddate>20060801</enddate><creator>Romero, Damian G</creator><creator>Plonczynski, Maria W</creator><creator>Gomez-Sanchez, Elise P</creator><creator>Yanes, Licy L</creator><creator>Gomez-Sanchez, Celso E</creator><general>Endocrine Society</general><general>Oxford University Press</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>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7U9</scope></search><sort><creationdate>20060801</creationdate><title>RGS2 Is Regulated by Angiotensin II and Functions as a Negative Feedback of Aldosterone Production in H295R Human Adrenocortical Cells</title><author>Romero, Damian G ; Plonczynski, Maria W ; Gomez-Sanchez, Elise P ; Yanes, Licy L ; Gomez-Sanchez, Celso E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c558t-c1ce2b9bb86370987823287fe1c924c32fa79152ef4b6dfd16f54cd9978d4463</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adrenal Cortex - cytology</topic><topic>Adrenal Cortex - metabolism</topic><topic>Adrenal Cortex - secretion</topic><topic>Adrenal glands</topic><topic>Aldosterone</topic><topic>Aldosterone - biosynthesis</topic><topic>Aldosterone - metabolism</topic><topic>Aldosterone - secretion</topic><topic>Aldosterone synthase</topic><topic>Angiotensin</topic><topic>Angiotensin II</topic><topic>Angiotensin II - metabolism</topic><topic>Angiotensin II - pharmacology</topic><topic>Antagonists</topic><topic>Biological and medical sciences</topic><topic>Calcimycin</topic><topic>Calcium antagonists</topic><topic>Calcium channel blockers</topic><topic>Calcium channels</topic><topic>Calcium ionophores</topic><topic>Calcium Signaling - drug effects</topic><topic>Calcium Signaling - physiology</topic><topic>Calcium-Calmodulin-Dependent Protein Kinases - metabolism</topic><topic>Calmodulin</topic><topic>Calmodulin - metabolism</topic><topic>Cell Line</topic><topic>Cell proliferation</topic><topic>Cytochrome P-450 CYP11B2 - metabolism</topic><topic>Deregulation</topic><topic>Feedback, Physiological - physiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression - drug effects</topic><topic>Gene Expression - physiology</topic><topic>Humans</topic><topic>Intracellular</topic><topic>Intracellular signalling</topic><topic>Kinases</topic><topic>mRNA</topic><topic>Negative feedback</topic><topic>Nifedipine</topic><topic>Protein Kinase C - metabolism</topic><topic>Proteins</topic><topic>Real time</topic><topic>Receptors</topic><topic>RGS Proteins - genetics</topic><topic>RGS Proteins - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>Secretion</topic><topic>Steroid 11-beta-Hydroxylase - metabolism</topic><topic>Steroidogenesis</topic><topic>Up-Regulation - drug effects</topic><topic>Up-Regulation - physiology</topic><topic>Vasoconstrictor Agents - metabolism</topic><topic>Vasoconstrictor Agents - pharmacology</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Romero, Damian G</creatorcontrib><creatorcontrib>Plonczynski, Maria W</creatorcontrib><creatorcontrib>Gomez-Sanchez, Elise P</creatorcontrib><creatorcontrib>Yanes, Licy L</creatorcontrib><creatorcontrib>Gomez-Sanchez, Celso E</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>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Virology and AIDS Abstracts</collection><jtitle>Endocrinology (Philadelphia)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Romero, Damian G</au><au>Plonczynski, Maria W</au><au>Gomez-Sanchez, Elise P</au><au>Yanes, Licy L</au><au>Gomez-Sanchez, Celso E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>RGS2 Is Regulated by Angiotensin II and Functions as a Negative Feedback of Aldosterone Production in H295R Human Adrenocortical Cells</atitle><jtitle>Endocrinology (Philadelphia)</jtitle><addtitle>Endocrinology</addtitle><date>2006-08-01</date><risdate>2006</risdate><volume>147</volume><issue>8</issue><spage>3889</spage><epage>3897</epage><pages>3889-3897</pages><issn>0013-7227</issn><eissn>1945-7170</eissn><coden>ENDOAO</coden><abstract>Regulator of G protein signaling (RGS) proteins interact with Gα-subunits of heterotrimeric G proteins, accelerating the rate of GTP hydrolysis and finalizing the intracellular signaling triggered by the G protein-coupled receptor-ligand interaction. Angiotensin (Ang) II interacts with its G protein-coupled receptor in zona glomerulosa adrenal cells and triggers a cascade of intracellular signals that regulates steroidogenesis and proliferation. We studied Ang II-mediated regulation of RGS2, the role of RGS2 in steroidogenesis, and the intracellular signal events involved in H295R human adrenal cells. We report that both H295R cells and human adrenal gland express RGS2 mRNA. In H295R cells, Ang II caused a rapid and transient increase in RGS2 mRNA levels quantified by real-time RT-PCR. Ang II effects were mimicked by calcium ionophore A23187 and blocked by calcium channel blocker nifedipine. Ang II effects also were blocked by calmodulin antagonists (W-7 and calmidazolium) and calcium/calmodulin-dependent kinase antagonist KN-93. RGS2 overexpression by retroviral infection in H295R cells caused a decrease in Ang II-stimulated aldosterone secretion but did not modify cortisol secretion. In reporter assays, RGS2 decreased Ang II-mediated aldosterone synthase up-regulation. These results suggest that Ang II up-regulates RGS2 mRNA by the calcium/calmodulin-dependent kinase pathway in H295R cells. RGS2 overexpression specifically decreases aldosterone secretion through a decrease in Ang II-mediated aldosterone synthase-induced expression. In conclusion, RGS2 expression is induced by Ang II to terminate the intracellular signaling cascade generated by Ang II. RGS2 alterations in expression levels or functionality could be implicated in deregulations of Ang II signaling and abnormal aldosterone secretion by the adrenal gland.</abstract><cop>Bethesda, MD</cop><pub>Endocrine Society</pub><pmid>16627589</pmid><doi>10.1210/en.2005-1532</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Adrenal Cortex - cytology Adrenal Cortex - metabolism Adrenal Cortex - secretion Adrenal glands Aldosterone Aldosterone - biosynthesis Aldosterone - metabolism Aldosterone - secretion Aldosterone synthase Angiotensin Angiotensin II Angiotensin II - metabolism Angiotensin II - pharmacology Antagonists Biological and medical sciences Calcimycin Calcium antagonists Calcium channel blockers Calcium channels Calcium ionophores Calcium Signaling - drug effects Calcium Signaling - physiology Calcium-Calmodulin-Dependent Protein Kinases - metabolism Calmodulin Calmodulin - metabolism Cell Line Cell proliferation Cytochrome P-450 CYP11B2 - metabolism Deregulation Feedback, Physiological - physiology Fundamental and applied biological sciences. Psychology Gene Expression - drug effects Gene Expression - physiology Humans Intracellular Intracellular signalling Kinases mRNA Negative feedback Nifedipine Protein Kinase C - metabolism Proteins Real time Receptors RGS Proteins - genetics RGS Proteins - metabolism RNA, Messenger - metabolism Secretion Steroid 11-beta-Hydroxylase - metabolism Steroidogenesis Up-Regulation - drug effects Up-Regulation - physiology Vasoconstrictor Agents - metabolism Vasoconstrictor Agents - pharmacology Vertebrates: endocrinology |
| title | RGS2 Is Regulated by Angiotensin II and Functions as a Negative Feedback of Aldosterone Production in H295R Human Adrenocortical Cells |
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