Brain-specific Restoration of Angiotensin II Corrects Renal Defects Seen in Angiotensinogen-deficient Mice
Mice deficient for angiotensinogen (AGT), or other components of the renin-angiotensin system, show a high rate of neonatal mortality correlated with severe renal abnormalities including hydronephrosis, hypertrophy of renal arteries, and an impaired ability to concentrate urine. Although transgenic...
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| Veröffentlicht in: | The Journal of biological chemistry 2003-01, Vol.278 (4), p.2184-2189 |
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| container_title | The Journal of biological chemistry |
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| creator | Lochard, Nadheige Silversides, David W van Kats, Jorge P Mercure, Chantal Reudelhuber, Timothy L |
| description | Mice deficient for angiotensinogen (AGT), or other components of the renin-angiotensin system, show a high rate of neonatal
mortality correlated with severe renal abnormalities including hydronephrosis, hypertrophy of renal arteries, and an impaired
ability to concentrate urine. Although transgenic replacement of systemic or adipose, but not renal, AGT in AGT-deficient
mice has previously been reported to correct some of these renal abnormalities, the tissue target for this complementation
has not been defined. In the current study, we have used a novel transgenic strategy to restore the peptide product of the
renin-angiotensin system, angiotensin II, exclusively in the brain of AGT-deficient mice and demonstrate that brain-specific
angiotensin II can correct the hydronephrosis and partially correct renal dysfunction seen in AGT-deficient mice. Taken together,
these results suggest that the renin-angiotensin system affects renal development and function through systemically accessible
targets in the brain. |
| doi_str_mv | 10.1074/jbc.M209933200 |
| format | Article |
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mortality correlated with severe renal abnormalities including hydronephrosis, hypertrophy of renal arteries, and an impaired
ability to concentrate urine. Although transgenic replacement of systemic or adipose, but not renal, AGT in AGT-deficient
mice has previously been reported to correct some of these renal abnormalities, the tissue target for this complementation
has not been defined. In the current study, we have used a novel transgenic strategy to restore the peptide product of the
renin-angiotensin system, angiotensin II, exclusively in the brain of AGT-deficient mice and demonstrate that brain-specific
angiotensin II can correct the hydronephrosis and partially correct renal dysfunction seen in AGT-deficient mice. Taken together,
these results suggest that the renin-angiotensin system affects renal development and function through systemically accessible
targets in the brain.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.M209933200</identifier><identifier>PMID: 12399452</identifier><language>eng</language><publisher>United States: American Society for Biochemistry and Molecular Biology</publisher><subject>Angiotensin II - biosynthesis ; Angiotensin II - metabolism ; Angiotensinogen - genetics ; Angiotensinogen - physiology ; Animals ; Blood Pressure ; Brain - metabolism ; Genetic Vectors ; Kidney - metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Radioimmunoassay ; Ribonucleases - metabolism ; RNA - metabolism ; Time Factors ; Water - metabolism</subject><ispartof>The Journal of biological chemistry, 2003-01, Vol.278 (4), p.2184-2189</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c389t-d47524a3d973ed62ae9275a7f8e748057d64200ccfcb55c8baa8d257f3ea48823</citedby><cites>FETCH-LOGICAL-c389t-d47524a3d973ed62ae9275a7f8e748057d64200ccfcb55c8baa8d257f3ea48823</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12399452$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lochard, Nadheige</creatorcontrib><creatorcontrib>Silversides, David W</creatorcontrib><creatorcontrib>van Kats, Jorge P</creatorcontrib><creatorcontrib>Mercure, Chantal</creatorcontrib><creatorcontrib>Reudelhuber, Timothy L</creatorcontrib><title>Brain-specific Restoration of Angiotensin II Corrects Renal Defects Seen in Angiotensinogen-deficient Mice</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>Mice deficient for angiotensinogen (AGT), or other components of the renin-angiotensin system, show a high rate of neonatal
mortality correlated with severe renal abnormalities including hydronephrosis, hypertrophy of renal arteries, and an impaired
ability to concentrate urine. Although transgenic replacement of systemic or adipose, but not renal, AGT in AGT-deficient
mice has previously been reported to correct some of these renal abnormalities, the tissue target for this complementation
has not been defined. In the current study, we have used a novel transgenic strategy to restore the peptide product of the
renin-angiotensin system, angiotensin II, exclusively in the brain of AGT-deficient mice and demonstrate that brain-specific
angiotensin II can correct the hydronephrosis and partially correct renal dysfunction seen in AGT-deficient mice. Taken together,
these results suggest that the renin-angiotensin system affects renal development and function through systemically accessible
targets in the brain.</description><subject>Angiotensin II - biosynthesis</subject><subject>Angiotensin II - metabolism</subject><subject>Angiotensinogen - genetics</subject><subject>Angiotensinogen - physiology</subject><subject>Animals</subject><subject>Blood Pressure</subject><subject>Brain - metabolism</subject><subject>Genetic Vectors</subject><subject>Kidney - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Mice, Transgenic</subject><subject>Radioimmunoassay</subject><subject>Ribonucleases - metabolism</subject><subject>RNA - metabolism</subject><subject>Time Factors</subject><subject>Water - metabolism</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0UtrGzEUBWBRUmrX7TbLMGSR3Th6WtLScdLWYBNIU-hOaDR3bBlbcqQxof8-Sm1wd9VGCD4duPcgdEnwmGDJbzeNGy8p1poxivEHNCRYsZoJ8vsCDTGmpNZUqAH6nPMGl8M1-YQGhDKtuaBDtLlL1oc678H5zrvqCXIfk-19DFXsqmlY-dhDyD5U83k1iymB63NhwW6re-j-vn4ChKqIf3RcQahbKJEeQl8tvYMv6GNntxm-nu4R-vXt4Xn2o148fp_PpovaMaX7uuVSUG5ZqyWDdkItaCqFlZ0CyRUWsp3wMqpznWuEcKqxVrVUyI6B5UpRNkI3x9x9ii-HMo_Z-exgu7UB4iEbSbXkkrL_QqImrCyMFzg-Qpdizgk6s09-Z9MfQ7B5r8GUGsy5hvLh6pR8aHbQnvlp7wVcH8Har9avPoFpfHRr2BkqleGGEsXZG3O-jyc</recordid><startdate>20030124</startdate><enddate>20030124</enddate><creator>Lochard, Nadheige</creator><creator>Silversides, David W</creator><creator>van Kats, Jorge P</creator><creator>Mercure, Chantal</creator><creator>Reudelhuber, Timothy L</creator><general>American Society for Biochemistry and Molecular Biology</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>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20030124</creationdate><title>Brain-specific Restoration of Angiotensin II Corrects Renal Defects Seen in Angiotensinogen-deficient Mice</title><author>Lochard, Nadheige ; Silversides, David W ; van Kats, Jorge P ; Mercure, Chantal ; Reudelhuber, Timothy L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c389t-d47524a3d973ed62ae9275a7f8e748057d64200ccfcb55c8baa8d257f3ea48823</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Angiotensin II - biosynthesis</topic><topic>Angiotensin II - metabolism</topic><topic>Angiotensinogen - genetics</topic><topic>Angiotensinogen - physiology</topic><topic>Animals</topic><topic>Blood Pressure</topic><topic>Brain - metabolism</topic><topic>Genetic Vectors</topic><topic>Kidney - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Mice, Transgenic</topic><topic>Radioimmunoassay</topic><topic>Ribonucleases - metabolism</topic><topic>RNA - metabolism</topic><topic>Time Factors</topic><topic>Water - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lochard, Nadheige</creatorcontrib><creatorcontrib>Silversides, David W</creatorcontrib><creatorcontrib>van Kats, Jorge P</creatorcontrib><creatorcontrib>Mercure, Chantal</creatorcontrib><creatorcontrib>Reudelhuber, Timothy L</creatorcontrib><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>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lochard, Nadheige</au><au>Silversides, David W</au><au>van Kats, Jorge P</au><au>Mercure, Chantal</au><au>Reudelhuber, Timothy L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Brain-specific Restoration of Angiotensin II Corrects Renal Defects Seen in Angiotensinogen-deficient Mice</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>2003-01-24</date><risdate>2003</risdate><volume>278</volume><issue>4</issue><spage>2184</spage><epage>2189</epage><pages>2184-2189</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><abstract>Mice deficient for angiotensinogen (AGT), or other components of the renin-angiotensin system, show a high rate of neonatal
mortality correlated with severe renal abnormalities including hydronephrosis, hypertrophy of renal arteries, and an impaired
ability to concentrate urine. Although transgenic replacement of systemic or adipose, but not renal, AGT in AGT-deficient
mice has previously been reported to correct some of these renal abnormalities, the tissue target for this complementation
has not been defined. In the current study, we have used a novel transgenic strategy to restore the peptide product of the
renin-angiotensin system, angiotensin II, exclusively in the brain of AGT-deficient mice and demonstrate that brain-specific
angiotensin II can correct the hydronephrosis and partially correct renal dysfunction seen in AGT-deficient mice. Taken together,
these results suggest that the renin-angiotensin system affects renal development and function through systemically accessible
targets in the brain.</abstract><cop>United States</cop><pub>American Society for Biochemistry and Molecular Biology</pub><pmid>12399452</pmid><doi>10.1074/jbc.M209933200</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 0021-9258 1083-351X |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Angiotensin II - biosynthesis Angiotensin II - metabolism Angiotensinogen - genetics Angiotensinogen - physiology Animals Blood Pressure Brain - metabolism Genetic Vectors Kidney - metabolism Mice Mice, Inbred C57BL Mice, Knockout Mice, Transgenic Radioimmunoassay Ribonucleases - metabolism RNA - metabolism Time Factors Water - metabolism |
| title | Brain-specific Restoration of Angiotensin II Corrects Renal Defects Seen in Angiotensinogen-deficient Mice |
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