Angiotensin II regulates parathyroid hormone-related protein expression in cultured rat aortic smooth muscle cells through transcriptional and post-transcriptional mechanisms
Parathyroid hormone-related protein (PTHrP), a tumor product responsible for malignancy-associated hypercalcemia, is also produced in many normal tissues, including vascular smooth muscle cells (SMC). As PTHrP exhibits vasodilatory properties, we postulated that other vasoactive agents may control P...
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| Veröffentlicht in: | The Journal of biological chemistry 1993-01, Vol.268 (3), p.1987-1994 |
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| container_end_page | 1994 |
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| container_issue | 3 |
| container_start_page | 1987 |
| container_title | The Journal of biological chemistry |
| container_volume | 268 |
| creator | PIROLA, C. J HAI-MEI WANG KAMYAR, A SIAOXING WU ENOMOTO, H SHARIFI, B FORRESTER, J. S CLEMENS, T. L FAGIN, J. A |
| description | Parathyroid hormone-related protein (PTHrP), a tumor product responsible for malignancy-associated hypercalcemia, is also
produced in many normal tissues, including vascular smooth muscle cells (SMC). As PTHrP exhibits vasodilatory properties,
we postulated that other vasoactive agents may control PTHrP gene expression in SMC. Addition of angiotensin II to serum-deprived
SMC resulted in a marked induction of PTHrP mRNA by 2 h, with a peak (6-10-fold) at 4-6 h. Angiotensin II effects on PTHrP
gene expression were inhibited by saralasin, an angiotensin II receptor antagonist, and blocked by actinomycin D and cycloheximide,
suggesting a requirement for gene transcription and protein synthesis. Nuclear run-off assays revealed a 3-fold increase in
PTHrP gene transcription 1 h after angiotensin II treatment. Angiotensin II also prolonged PTHrP mRNA half-life by 2-3-fold.
Angiotensin-induced PTHrP mRNA is partially dependent on cyclooxygenase products and protein kinase C activation. Other vasoconstrictor
substances, including serotonin and bradykinin, also stimulated PTHrP expression, whereas the vasodilator atrial natriuretic
peptide did not. Addition of recombinant PTHrP-(1-141) significantly inhibited angiotensin II-induced SMC DNA synthesis. PTHrP
expression is increased by angiotensin II through transcriptional and post-transcriptional mechanisms. In addition, PTHrP
modulates the effect of angiotensin II on SMC proliferation. This suggests that PTHrP acts locally in SMC, possibly to oppose
the vasoactive and/or growth-promoting effects of vasoconstrictor agents such as angiotensin II. |
| doi_str_mv | 10.1016/s0021-9258(18)53952-1 |
| format | Article |
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produced in many normal tissues, including vascular smooth muscle cells (SMC). As PTHrP exhibits vasodilatory properties,
we postulated that other vasoactive agents may control PTHrP gene expression in SMC. Addition of angiotensin II to serum-deprived
SMC resulted in a marked induction of PTHrP mRNA by 2 h, with a peak (6-10-fold) at 4-6 h. Angiotensin II effects on PTHrP
gene expression were inhibited by saralasin, an angiotensin II receptor antagonist, and blocked by actinomycin D and cycloheximide,
suggesting a requirement for gene transcription and protein synthesis. Nuclear run-off assays revealed a 3-fold increase in
PTHrP gene transcription 1 h after angiotensin II treatment. Angiotensin II also prolonged PTHrP mRNA half-life by 2-3-fold.
Angiotensin-induced PTHrP mRNA is partially dependent on cyclooxygenase products and protein kinase C activation. Other vasoconstrictor
substances, including serotonin and bradykinin, also stimulated PTHrP expression, whereas the vasodilator atrial natriuretic
peptide did not. Addition of recombinant PTHrP-(1-141) significantly inhibited angiotensin II-induced SMC DNA synthesis. PTHrP
expression is increased by angiotensin II through transcriptional and post-transcriptional mechanisms. In addition, PTHrP
modulates the effect of angiotensin II on SMC proliferation. This suggests that PTHrP acts locally in SMC, possibly to oppose
the vasoactive and/or growth-promoting effects of vasoconstrictor agents such as angiotensin II.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1016/s0021-9258(18)53952-1</identifier><identifier>PMID: 8420973</identifier><identifier>CODEN: JBCHA3</identifier><language>eng</language><publisher>Bethesda, MD: American Society for Biochemistry and Molecular Biology</publisher><subject>Angiotensin II - pharmacology ; Animals ; Aorta ; Biological and medical sciences ; Blood ; Cells, Cultured ; Cycloheximide - pharmacology ; Dactinomycin - pharmacology ; DNA - biosynthesis ; Fundamental and applied biological sciences. Psychology ; Gene Expression Regulation - drug effects ; Kinetics ; Male ; Molecular and cellular biology ; Molecular genetics ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - metabolism ; Parathyroid Hormone-Related Protein ; Proteins - genetics ; Proto-Oncogenes - genetics ; Rats ; Rats, Sprague-Dawley ; RNA, Messenger - biosynthesis ; Second Messenger Systems ; Transcription, Genetic - drug effects ; Transcription. Transcription factor. Splicing. Rna processing</subject><ispartof>The Journal of biological chemistry, 1993-01, Vol.268 (3), p.1987-1994</ispartof><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4191-f68f0fe04288130f814db9b8154312a6d629ca599fa3e759afe843117c0c45943</citedby><cites>FETCH-LOGICAL-c4191-f68f0fe04288130f814db9b8154312a6d629ca599fa3e759afe843117c0c45943</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4580744$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8420973$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>PIROLA, C. J</creatorcontrib><creatorcontrib>HAI-MEI WANG</creatorcontrib><creatorcontrib>KAMYAR, A</creatorcontrib><creatorcontrib>SIAOXING WU</creatorcontrib><creatorcontrib>ENOMOTO, H</creatorcontrib><creatorcontrib>SHARIFI, B</creatorcontrib><creatorcontrib>FORRESTER, J. S</creatorcontrib><creatorcontrib>CLEMENS, T. L</creatorcontrib><creatorcontrib>FAGIN, J. A</creatorcontrib><title>Angiotensin II regulates parathyroid hormone-related protein expression in cultured rat aortic smooth muscle cells through transcriptional and post-transcriptional mechanisms</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>Parathyroid hormone-related protein (PTHrP), a tumor product responsible for malignancy-associated hypercalcemia, is also
produced in many normal tissues, including vascular smooth muscle cells (SMC). As PTHrP exhibits vasodilatory properties,
we postulated that other vasoactive agents may control PTHrP gene expression in SMC. Addition of angiotensin II to serum-deprived
SMC resulted in a marked induction of PTHrP mRNA by 2 h, with a peak (6-10-fold) at 4-6 h. Angiotensin II effects on PTHrP
gene expression were inhibited by saralasin, an angiotensin II receptor antagonist, and blocked by actinomycin D and cycloheximide,
suggesting a requirement for gene transcription and protein synthesis. Nuclear run-off assays revealed a 3-fold increase in
PTHrP gene transcription 1 h after angiotensin II treatment. Angiotensin II also prolonged PTHrP mRNA half-life by 2-3-fold.
Angiotensin-induced PTHrP mRNA is partially dependent on cyclooxygenase products and protein kinase C activation. Other vasoconstrictor
substances, including serotonin and bradykinin, also stimulated PTHrP expression, whereas the vasodilator atrial natriuretic
peptide did not. Addition of recombinant PTHrP-(1-141) significantly inhibited angiotensin II-induced SMC DNA synthesis. PTHrP
expression is increased by angiotensin II through transcriptional and post-transcriptional mechanisms. In addition, PTHrP
modulates the effect of angiotensin II on SMC proliferation. This suggests that PTHrP acts locally in SMC, possibly to oppose
the vasoactive and/or growth-promoting effects of vasoconstrictor agents such as angiotensin II.</description><subject>Angiotensin II - pharmacology</subject><subject>Animals</subject><subject>Aorta</subject><subject>Biological and medical sciences</subject><subject>Blood</subject><subject>Cells, Cultured</subject><subject>Cycloheximide - pharmacology</subject><subject>Dactinomycin - pharmacology</subject><subject>DNA - biosynthesis</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Kinetics</subject><subject>Male</subject><subject>Molecular and cellular biology</subject><subject>Molecular genetics</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - metabolism</subject><subject>Parathyroid Hormone-Related Protein</subject><subject>Proteins - genetics</subject><subject>Proto-Oncogenes - genetics</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>RNA, Messenger - biosynthesis</subject><subject>Second Messenger Systems</subject><subject>Transcription, Genetic - drug effects</subject><subject>Transcription. Transcription factor. Splicing. Rna processing</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkVGL1DAUhYMo6-zqT1gIIqIP1dwmaZPHZdF1YMEHFXwLmTSdRtpmzE1x90_5G02dYR7MSwjfOSc3OYRcA3sPDJoPyFgNla6legvqneRa1hU8IRtgildcwo-nZHOWPCeXiD9ZWULDBblQoma65Rvy52beh5j9jGGm2y1Nfr-MNnukB5tsHh5TDB0dYpri7KvkV9bRQyqWYvAPh-QRQ5xpObllzEsquBipjSkHR3GKMQ90WtCNnjo_jkjzkOKyH2hOdkaXwiGXADtSO5fkiLn6H0zeDXYOOOEL8qy3I_qXp_2KfP_08dvt5-r-y9329ua-cgI0VH2jetZ7JmqlgLNegeh2eqdACg61bbqm1s5KrXvLfSu17b0qBFrHnJBa8Cvy5phbXvpr8ZjNFHCd3s4-LmigES1vW12E8ih0KSIm35tDCpNNjwaYWXsyX9cSzFqCAWX-9WSg-K5PFyy7yXdn16mYwl-fuEVnx778iAt4lgmpWCvWOV8dZUPYD79D8mYXohv8ZOpGGW5Aq5b_BaTYq9c</recordid><startdate>19930125</startdate><enddate>19930125</enddate><creator>PIROLA, C. J</creator><creator>HAI-MEI WANG</creator><creator>KAMYAR, A</creator><creator>SIAOXING WU</creator><creator>ENOMOTO, H</creator><creator>SHARIFI, B</creator><creator>FORRESTER, J. S</creator><creator>CLEMENS, T. L</creator><creator>FAGIN, J. A</creator><general>American Society for Biochemistry and Molecular Biology</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>7TM</scope></search><sort><creationdate>19930125</creationdate><title>Angiotensin II regulates parathyroid hormone-related protein expression in cultured rat aortic smooth muscle cells through transcriptional and post-transcriptional mechanisms</title><author>PIROLA, C. J ; HAI-MEI WANG ; KAMYAR, A ; SIAOXING WU ; ENOMOTO, H ; SHARIFI, B ; FORRESTER, J. S ; CLEMENS, T. L ; FAGIN, J. A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4191-f68f0fe04288130f814db9b8154312a6d629ca599fa3e759afe843117c0c45943</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Angiotensin II - pharmacology</topic><topic>Animals</topic><topic>Aorta</topic><topic>Biological and medical sciences</topic><topic>Blood</topic><topic>Cells, Cultured</topic><topic>Cycloheximide - pharmacology</topic><topic>Dactinomycin - pharmacology</topic><topic>DNA - biosynthesis</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Kinetics</topic><topic>Male</topic><topic>Molecular and cellular biology</topic><topic>Molecular genetics</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - metabolism</topic><topic>Parathyroid Hormone-Related Protein</topic><topic>Proteins - genetics</topic><topic>Proto-Oncogenes - genetics</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>RNA, Messenger - biosynthesis</topic><topic>Second Messenger Systems</topic><topic>Transcription, Genetic - drug effects</topic><topic>Transcription. Transcription factor. Splicing. Rna processing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>PIROLA, C. J</creatorcontrib><creatorcontrib>HAI-MEI WANG</creatorcontrib><creatorcontrib>KAMYAR, A</creatorcontrib><creatorcontrib>SIAOXING WU</creatorcontrib><creatorcontrib>ENOMOTO, H</creatorcontrib><creatorcontrib>SHARIFI, B</creatorcontrib><creatorcontrib>FORRESTER, J. S</creatorcontrib><creatorcontrib>CLEMENS, T. L</creatorcontrib><creatorcontrib>FAGIN, J. A</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>Nucleic Acids Abstracts</collection><jtitle>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>PIROLA, C. J</au><au>HAI-MEI WANG</au><au>KAMYAR, A</au><au>SIAOXING WU</au><au>ENOMOTO, H</au><au>SHARIFI, B</au><au>FORRESTER, J. S</au><au>CLEMENS, T. L</au><au>FAGIN, J. A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Angiotensin II regulates parathyroid hormone-related protein expression in cultured rat aortic smooth muscle cells through transcriptional and post-transcriptional mechanisms</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>1993-01-25</date><risdate>1993</risdate><volume>268</volume><issue>3</issue><spage>1987</spage><epage>1994</epage><pages>1987-1994</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><coden>JBCHA3</coden><abstract>Parathyroid hormone-related protein (PTHrP), a tumor product responsible for malignancy-associated hypercalcemia, is also
produced in many normal tissues, including vascular smooth muscle cells (SMC). As PTHrP exhibits vasodilatory properties,
we postulated that other vasoactive agents may control PTHrP gene expression in SMC. Addition of angiotensin II to serum-deprived
SMC resulted in a marked induction of PTHrP mRNA by 2 h, with a peak (6-10-fold) at 4-6 h. Angiotensin II effects on PTHrP
gene expression were inhibited by saralasin, an angiotensin II receptor antagonist, and blocked by actinomycin D and cycloheximide,
suggesting a requirement for gene transcription and protein synthesis. Nuclear run-off assays revealed a 3-fold increase in
PTHrP gene transcription 1 h after angiotensin II treatment. Angiotensin II also prolonged PTHrP mRNA half-life by 2-3-fold.
Angiotensin-induced PTHrP mRNA is partially dependent on cyclooxygenase products and protein kinase C activation. Other vasoconstrictor
substances, including serotonin and bradykinin, also stimulated PTHrP expression, whereas the vasodilator atrial natriuretic
peptide did not. Addition of recombinant PTHrP-(1-141) significantly inhibited angiotensin II-induced SMC DNA synthesis. PTHrP
expression is increased by angiotensin II through transcriptional and post-transcriptional mechanisms. In addition, PTHrP
modulates the effect of angiotensin II on SMC proliferation. This suggests that PTHrP acts locally in SMC, possibly to oppose
the vasoactive and/or growth-promoting effects of vasoconstrictor agents such as angiotensin II.</abstract><cop>Bethesda, MD</cop><pub>American Society for Biochemistry and Molecular Biology</pub><pmid>8420973</pmid><doi>10.1016/s0021-9258(18)53952-1</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 0021-9258 1083-351X |
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| subjects | Angiotensin II - pharmacology Animals Aorta Biological and medical sciences Blood Cells, Cultured Cycloheximide - pharmacology Dactinomycin - pharmacology DNA - biosynthesis Fundamental and applied biological sciences. Psychology Gene Expression Regulation - drug effects Kinetics Male Molecular and cellular biology Molecular genetics Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - metabolism Parathyroid Hormone-Related Protein Proteins - genetics Proto-Oncogenes - genetics Rats Rats, Sprague-Dawley RNA, Messenger - biosynthesis Second Messenger Systems Transcription, Genetic - drug effects Transcription. Transcription factor. Splicing. Rna processing |
| title | Angiotensin II regulates parathyroid hormone-related protein expression in cultured rat aortic smooth muscle cells through transcriptional and post-transcriptional mechanisms |
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