Inhibition and down-regulation of gene transcription and guanylyl cyclase activity of NPRA by angiotensin II involving protein kinase C
The objective of this study was to investigate the role of protein kinase C (PKC) in the angiotensin II (Ang II)-dependent repression of Npr1 (coding for natriuretic peptide receptor-A, NPRA) gene transcription. Mouse mesangial cells (MMCs) were transfected with Npr1 gene promoter-luciferase constru...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2006-10, Vol.349 (1), p.131-135 |
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| creator | Arise, Kiran K. Pandey, Kailash N. |
| description | The objective of this study was to investigate the role of protein kinase C (PKC) in the angiotensin II (Ang II)-dependent repression of
Npr1 (coding for natriuretic peptide receptor-A, NPRA) gene transcription. Mouse mesangial cells (MMCs) were transfected with
Npr1 gene promoter-luciferase construct and treated with Ang II and PKC agonist or antagonist. The results showed that the treatment of MMCs with 10
nM Ang II produced a 60% reduction in the promoter activity of
Npr1 gene. MMCs treated with 10
nM Ang II exhibited 55% reduction in NPRA mRNA levels, and subsequent stimulation with 100
nM ANP resulted in 50% reduction in guanylyl cyclase (GC) activity. Furthermore, the treatment of MMCs with Ang II in the presence of PKC agonist phorbol ester (100
nM) produced an almost 75% reduction in NPRA mRNA and 70% reduction in the intracellular accumulation of cGMP levels. PKC antagonist staurosporine completely reversed the effect of Ang II and phorbol ester. This is the first report to demonstrate that ANG II-dependent transcriptional repression of
Npr1 gene promoter activity and down-regulation of GC activity of translated protein, NPRA is regulated by PKC pathways. |
| doi_str_mv | 10.1016/j.bbrc.2006.08.003 |
| format | Article |
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Npr1 (coding for natriuretic peptide receptor-A, NPRA) gene transcription. Mouse mesangial cells (MMCs) were transfected with
Npr1 gene promoter-luciferase construct and treated with Ang II and PKC agonist or antagonist. The results showed that the treatment of MMCs with 10
nM Ang II produced a 60% reduction in the promoter activity of
Npr1 gene. MMCs treated with 10
nM Ang II exhibited 55% reduction in NPRA mRNA levels, and subsequent stimulation with 100
nM ANP resulted in 50% reduction in guanylyl cyclase (GC) activity. Furthermore, the treatment of MMCs with Ang II in the presence of PKC agonist phorbol ester (100
nM) produced an almost 75% reduction in NPRA mRNA and 70% reduction in the intracellular accumulation of cGMP levels. PKC antagonist staurosporine completely reversed the effect of Ang II and phorbol ester. This is the first report to demonstrate that ANG II-dependent transcriptional repression of
Npr1 gene promoter activity and down-regulation of GC activity of translated protein, NPRA is regulated by PKC pathways.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2006.08.003</identifier><identifier>PMID: 16930545</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Angiotensin II - physiology ; Animals ; Gene Expression Regulation, Enzymologic ; Gene transcription ; Guanylate Cyclase - metabolism ; Mesangial cells ; Mesangial Cells - cytology ; Mice ; Natriuretic peptide receptor ; Npr1 promoter ; Promoter Regions, Genetic ; Protein kinase C ; Protein Kinase C - metabolism ; Receptors, Atrial Natriuretic Factor - metabolism ; RNA, Messenger - metabolism ; Staurosporine - pharmacology ; Transcription, Genetic ; Transfection</subject><ispartof>Biochemical and biophysical research communications, 2006-10, Vol.349 (1), p.131-135</ispartof><rights>2006 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c451t-786fb0da1b24ca49f61e390ce705f71a02021ae337c6fe892f309b559799aa4b3</citedby><cites>FETCH-LOGICAL-c451t-786fb0da1b24ca49f61e390ce705f71a02021ae337c6fe892f309b559799aa4b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006291X06017876$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16930545$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Arise, Kiran K.</creatorcontrib><creatorcontrib>Pandey, Kailash N.</creatorcontrib><title>Inhibition and down-regulation of gene transcription and guanylyl cyclase activity of NPRA by angiotensin II involving protein kinase C</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>The objective of this study was to investigate the role of protein kinase C (PKC) in the angiotensin II (Ang II)-dependent repression of
Npr1 (coding for natriuretic peptide receptor-A, NPRA) gene transcription. Mouse mesangial cells (MMCs) were transfected with
Npr1 gene promoter-luciferase construct and treated with Ang II and PKC agonist or antagonist. The results showed that the treatment of MMCs with 10
nM Ang II produced a 60% reduction in the promoter activity of
Npr1 gene. MMCs treated with 10
nM Ang II exhibited 55% reduction in NPRA mRNA levels, and subsequent stimulation with 100
nM ANP resulted in 50% reduction in guanylyl cyclase (GC) activity. Furthermore, the treatment of MMCs with Ang II in the presence of PKC agonist phorbol ester (100
nM) produced an almost 75% reduction in NPRA mRNA and 70% reduction in the intracellular accumulation of cGMP levels. PKC antagonist staurosporine completely reversed the effect of Ang II and phorbol ester. This is the first report to demonstrate that ANG II-dependent transcriptional repression of
Npr1 gene promoter activity and down-regulation of GC activity of translated protein, NPRA is regulated by PKC pathways.</description><subject>Angiotensin II - physiology</subject><subject>Animals</subject><subject>Gene Expression Regulation, Enzymologic</subject><subject>Gene transcription</subject><subject>Guanylate Cyclase - metabolism</subject><subject>Mesangial cells</subject><subject>Mesangial Cells - cytology</subject><subject>Mice</subject><subject>Natriuretic peptide receptor</subject><subject>Npr1 promoter</subject><subject>Promoter Regions, Genetic</subject><subject>Protein kinase C</subject><subject>Protein Kinase C - metabolism</subject><subject>Receptors, Atrial Natriuretic Factor - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>Staurosporine - pharmacology</subject><subject>Transcription, Genetic</subject><subject>Transfection</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc2q1DAYhoMonjlHb8CFZOWu9Ut_0gTcHAb1DBxURMFdSNKvNWMnHZN2pFfgbZs6g-50FXjzvC8hDyHPGOQMGH-5z40JNi8AeA4iBygfkA0DCVnBoHpINpBuskKyL1fkOsY9AGMVl4_JFeOyhLqqN-Tnzn91xk1u9FT7lrbjD58F7OdB_87GjvbokU5B-2iDO_4h-1n7ZVgGahc76IhU28md3LSsnXcfPt5SsySwd-OEPjpPdzvq_GkcTs739BhSnMJvzq_d7RPyqNNDxKeX84Z8fvP60_Yuu3__dre9vc9sVbMpawTvDLSamaKyupIdZ1hKsNhA3TVMQwEF01iWjeUdCll0JUhT17KRUuvKlDfkxXk3PeD7jHFSBxctDoP2OM5RcSEqIQT_L8hkKXgNIoHFGbRhjDFgp47BHXRYFAO1elJ7tXpSqycFQiVPqfT8sj6bA7Z_KxcxCXh1BjB9xslhUNE69BZbF9BOqh3dv_Z_AeDspdw</recordid><startdate>20061013</startdate><enddate>20061013</enddate><creator>Arise, Kiran K.</creator><creator>Pandey, Kailash N.</creator><general>Elsevier Inc</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><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20061013</creationdate><title>Inhibition and down-regulation of gene transcription and guanylyl cyclase activity of NPRA by angiotensin II involving protein kinase C</title><author>Arise, Kiran K. ; Pandey, Kailash N.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c451t-786fb0da1b24ca49f61e390ce705f71a02021ae337c6fe892f309b559799aa4b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Angiotensin II - physiology</topic><topic>Animals</topic><topic>Gene Expression Regulation, Enzymologic</topic><topic>Gene transcription</topic><topic>Guanylate Cyclase - metabolism</topic><topic>Mesangial cells</topic><topic>Mesangial Cells - cytology</topic><topic>Mice</topic><topic>Natriuretic peptide receptor</topic><topic>Npr1 promoter</topic><topic>Promoter Regions, Genetic</topic><topic>Protein kinase C</topic><topic>Protein Kinase C - metabolism</topic><topic>Receptors, Atrial Natriuretic Factor - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>Staurosporine - pharmacology</topic><topic>Transcription, Genetic</topic><topic>Transfection</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Arise, Kiran K.</creatorcontrib><creatorcontrib>Pandey, Kailash N.</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><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Arise, Kiran K.</au><au>Pandey, Kailash N.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition and down-regulation of gene transcription and guanylyl cyclase activity of NPRA by angiotensin II involving protein kinase C</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2006-10-13</date><risdate>2006</risdate><volume>349</volume><issue>1</issue><spage>131</spage><epage>135</epage><pages>131-135</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>The objective of this study was to investigate the role of protein kinase C (PKC) in the angiotensin II (Ang II)-dependent repression of
Npr1 (coding for natriuretic peptide receptor-A, NPRA) gene transcription. Mouse mesangial cells (MMCs) were transfected with
Npr1 gene promoter-luciferase construct and treated with Ang II and PKC agonist or antagonist. The results showed that the treatment of MMCs with 10
nM Ang II produced a 60% reduction in the promoter activity of
Npr1 gene. MMCs treated with 10
nM Ang II exhibited 55% reduction in NPRA mRNA levels, and subsequent stimulation with 100
nM ANP resulted in 50% reduction in guanylyl cyclase (GC) activity. Furthermore, the treatment of MMCs with Ang II in the presence of PKC agonist phorbol ester (100
nM) produced an almost 75% reduction in NPRA mRNA and 70% reduction in the intracellular accumulation of cGMP levels. PKC antagonist staurosporine completely reversed the effect of Ang II and phorbol ester. This is the first report to demonstrate that ANG II-dependent transcriptional repression of
Npr1 gene promoter activity and down-regulation of GC activity of translated protein, NPRA is regulated by PKC pathways.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>16930545</pmid><doi>10.1016/j.bbrc.2006.08.003</doi><tpages>5</tpages></addata></record> |
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| ispartof | Biochemical and biophysical research communications, 2006-10, Vol.349 (1), p.131-135 |
| issn | 0006-291X 1090-2104 |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Angiotensin II - physiology Animals Gene Expression Regulation, Enzymologic Gene transcription Guanylate Cyclase - metabolism Mesangial cells Mesangial Cells - cytology Mice Natriuretic peptide receptor Npr1 promoter Promoter Regions, Genetic Protein kinase C Protein Kinase C - metabolism Receptors, Atrial Natriuretic Factor - metabolism RNA, Messenger - metabolism Staurosporine - pharmacology Transcription, Genetic Transfection |
| title | Inhibition and down-regulation of gene transcription and guanylyl cyclase activity of NPRA by angiotensin II involving protein kinase C |
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