Plasminogen activator inhibitor-1 deficiency protects against aldosterone-induced glomerular injury
This study tests the hypothesis that plasminogen activator inhibitor-1 (PAI-1) contributes to aldosterone-induced renal and cardiac injury. The effects of 12-week aldosterone (2.8 μg/day)/salt (1% drinking water) versus vehicle/salt on renal and cardiac histology and mRNA expression were determined...
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| Veröffentlicht in: | Kidney international 2006-03, Vol.69 (6), p.1064-1072 |
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| creator | Ma, J. Weisberg, A. Griffin, J.P. Vaughan, D.E. Fogo, A.B. Brown, N.J. |
| description | This study tests the hypothesis that plasminogen activator inhibitor-1 (PAI-1) contributes to aldosterone-induced renal and cardiac injury. The effects of 12-week aldosterone (2.8 μg/day)/salt (1% drinking water) versus vehicle/salt on renal and cardiac histology and mRNA expression were determined in wild-type (WT) and PAI-1 deficient (PAI-1(−/−)) mice. Systolic blood pressure was similar in aldosterone-infused WT and PAI-1(−/−) mice until 12 weeks, when it was significantly higher in the WT mice. At 12 weeks, urine volume, sodium excretion, and sodium/potassium ratio were similarly increased in the two aldosterone-infused groups. In contrast, urine albumin excretion was greater in aldosterone-infused WT mice (mean±s.d.: 699.0±873.0 μg/24 h) compared to vehicle-infused WT (23.6±9.0 μg/24 h, P=0.003) or aldosterone-infused PAI-1(−/−) mice (131.6±110.6 μg/24 h, P=0.007). Aldosterone increased glomerular area to a greater extent in WT (4651±577 versus 3278±488 μm2/glomerulus in vehicle-infused WT, P |
| doi_str_mv | 10.1038/sj.ki.5000201 |
| format | Article |
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The effects of 12-week aldosterone (2.8 μg/day)/salt (1% drinking water) versus vehicle/salt on renal and cardiac histology and mRNA expression were determined in wild-type (WT) and PAI-1 deficient (PAI-1(−/−)) mice. Systolic blood pressure was similar in aldosterone-infused WT and PAI-1(−/−) mice until 12 weeks, when it was significantly higher in the WT mice. At 12 weeks, urine volume, sodium excretion, and sodium/potassium ratio were similarly increased in the two aldosterone-infused groups. In contrast, urine albumin excretion was greater in aldosterone-infused WT mice (mean±s.d.: 699.0±873.0 μg/24 h) compared to vehicle-infused WT (23.6±9.0 μg/24 h, P=0.003) or aldosterone-infused PAI-1(−/−) mice (131.6±110.6 μg/24 h, P=0.007). Aldosterone increased glomerular area to a greater extent in WT (4651±577 versus 3278±488 μm2/glomerulus in vehicle-infused WT, P<0.001) than in PAI-1(−/−) mice (3713±705 μm2/glomerulus, P=0.001 versus aldosterone-infused WT), with corresponding mesangial expansion. Renal collagen content was also increased in aldosterone-infused WT versus PAI-1(−/−) mice. In WT mice, aldosterone increased renal mRNA expression of PAI-1, collagen I, collagen III, osteopontin, fibronectin, monocyte chemoattractant protein-1 (MCP-1), and F4/80 (all P<0.05), but not transforming growth factor beta (TGF-β). In PAI-1(−/−) mice, aldosterone increased renal expression of collagen I, osteopontin, fibronectin, and MCP-1, and tended to increase collagen III. Renal osteopontin expression was diminished in aldosterone-treated PAI-1(−/−) compared to aldosterone-treated WT mice (P=0.05). Aldosterone induced cardiac hypertrophy but not fibrosis in WT and PAI-1(−/−) mice. PAI-1 contributes to aldosterone-induced glomerular injury.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1038/sj.ki.5000201</identifier><identifier>PMID: 16528256</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Albuminuria - urine ; aldosterone ; Aldosterone - adverse effects ; Aldosterone - pharmacology ; angiotensin ; Animals ; Biological and medical sciences ; Blood Pressure - drug effects ; Blood Pressure - physiology ; Chemokine CCL2 - analysis ; Chemokine CCL2 - genetics ; Collagen - analysis ; Collagen - genetics ; Fibronectins - analysis ; Fibronectins - genetics ; Gene Expression ; Glomerulonephritis ; Glomerulonephritis - chemically induced ; Glomerulonephritis - physiopathology ; Glomerulonephritis - prevention & control ; Glomerulonephritis - urine ; Hemodynamics - physiology ; Kidney Glomerulus - chemistry ; Kidney Glomerulus - drug effects ; Kidney Glomerulus - pathology ; Kidney Glomerulus - physiopathology ; Macrophages - pathology ; Male ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Myocardium - chemistry ; Myocardium - pathology ; Nephrectomy ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; Osteopontin ; Plasminogen Activator Inhibitor 1 - deficiency ; Plasminogen Activator Inhibitor 1 - genetics ; Plasminogen Activator Inhibitor 1 - physiology ; plasminogen activator inhibitor-1 ; RNA, Messenger - analysis ; Sialoglycoproteins - analysis ; Sialoglycoproteins - genetics ; Sodium - urine</subject><ispartof>Kidney international, 2006-03, Vol.69 (6), p.1064-1072</ispartof><rights>2006 International Society of Nephrology</rights><rights>2006 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Mar 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c501t-3e5dca9302835bf183854bf3a63283759dc6a1b0ff3c2bb2e9d0369e0915a69f3</citedby><cites>FETCH-LOGICAL-c501t-3e5dca9302835bf183854bf3a63283759dc6a1b0ff3c2bb2e9d0369e0915a69f3</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=17924207$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16528256$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ma, J.</creatorcontrib><creatorcontrib>Weisberg, A.</creatorcontrib><creatorcontrib>Griffin, J.P.</creatorcontrib><creatorcontrib>Vaughan, D.E.</creatorcontrib><creatorcontrib>Fogo, A.B.</creatorcontrib><creatorcontrib>Brown, N.J.</creatorcontrib><title>Plasminogen activator inhibitor-1 deficiency protects against aldosterone-induced glomerular injury</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>This study tests the hypothesis that plasminogen activator inhibitor-1 (PAI-1) contributes to aldosterone-induced renal and cardiac injury. The effects of 12-week aldosterone (2.8 μg/day)/salt (1% drinking water) versus vehicle/salt on renal and cardiac histology and mRNA expression were determined in wild-type (WT) and PAI-1 deficient (PAI-1(−/−)) mice. Systolic blood pressure was similar in aldosterone-infused WT and PAI-1(−/−) mice until 12 weeks, when it was significantly higher in the WT mice. At 12 weeks, urine volume, sodium excretion, and sodium/potassium ratio were similarly increased in the two aldosterone-infused groups. In contrast, urine albumin excretion was greater in aldosterone-infused WT mice (mean±s.d.: 699.0±873.0 μg/24 h) compared to vehicle-infused WT (23.6±9.0 μg/24 h, P=0.003) or aldosterone-infused PAI-1(−/−) mice (131.6±110.6 μg/24 h, P=0.007). Aldosterone increased glomerular area to a greater extent in WT (4651±577 versus 3278±488 μm2/glomerulus in vehicle-infused WT, P<0.001) than in PAI-1(−/−) mice (3713±705 μm2/glomerulus, P=0.001 versus aldosterone-infused WT), with corresponding mesangial expansion. Renal collagen content was also increased in aldosterone-infused WT versus PAI-1(−/−) mice. In WT mice, aldosterone increased renal mRNA expression of PAI-1, collagen I, collagen III, osteopontin, fibronectin, monocyte chemoattractant protein-1 (MCP-1), and F4/80 (all P<0.05), but not transforming growth factor beta (TGF-β). In PAI-1(−/−) mice, aldosterone increased renal expression of collagen I, osteopontin, fibronectin, and MCP-1, and tended to increase collagen III. Renal osteopontin expression was diminished in aldosterone-treated PAI-1(−/−) compared to aldosterone-treated WT mice (P=0.05). Aldosterone induced cardiac hypertrophy but not fibrosis in WT and PAI-1(−/−) mice. PAI-1 contributes to aldosterone-induced glomerular injury.</description><subject>Albuminuria - urine</subject><subject>aldosterone</subject><subject>Aldosterone - adverse effects</subject><subject>Aldosterone - pharmacology</subject><subject>angiotensin</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - drug effects</subject><subject>Blood Pressure - physiology</subject><subject>Chemokine CCL2 - analysis</subject><subject>Chemokine CCL2 - genetics</subject><subject>Collagen - analysis</subject><subject>Collagen - genetics</subject><subject>Fibronectins - analysis</subject><subject>Fibronectins - genetics</subject><subject>Gene Expression</subject><subject>Glomerulonephritis</subject><subject>Glomerulonephritis - chemically induced</subject><subject>Glomerulonephritis - physiopathology</subject><subject>Glomerulonephritis - prevention & control</subject><subject>Glomerulonephritis - urine</subject><subject>Hemodynamics - physiology</subject><subject>Kidney Glomerulus - chemistry</subject><subject>Kidney Glomerulus - drug effects</subject><subject>Kidney Glomerulus - pathology</subject><subject>Kidney Glomerulus - physiopathology</subject><subject>Macrophages - pathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Inbred Strains</subject><subject>Myocardium - chemistry</subject><subject>Myocardium - pathology</subject><subject>Nephrectomy</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><subject>Osteopontin</subject><subject>Plasminogen Activator Inhibitor 1 - deficiency</subject><subject>Plasminogen Activator Inhibitor 1 - genetics</subject><subject>Plasminogen Activator Inhibitor 1 - physiology</subject><subject>plasminogen activator inhibitor-1</subject><subject>RNA, Messenger - analysis</subject><subject>Sialoglycoproteins - analysis</subject><subject>Sialoglycoproteins - genetics</subject><subject>Sodium - urine</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kE1rGzEQhkVJqR23x1zDEshxnZFk7cexhKQtBJpDexZaaeRqvZZcaTfgf1-5XvAppxmGh3deHkJuKKwp8OYh9eudWwsAYEA_kCUVjJe0FuKKLAEaUTLBmwW5TqnPTNNy-EQWtBKsYaJaEv06qLR3PmzRF0qP7k2NIRbO_3Gdy1tJC4PWaYdeH4tDDCPqMRVqq5xPY6EGE9KIMXgsnTeTRlNsh7DHOA3qFNNP8fiZfLRqSPhlnivy-_np1-P38uXntx-PX19KLYCOJUdhtMoFWcNFZ2nDG7HpLFcVz5datEZXinZgLdes6xi2BnjVIrRUqKq1fEXuzrm55t8J0yj7MEWfX0pGgVKoeJ2h8gzpGFKKaOUhur2KR0lBnozK1Mudk7PRzN_OoVO3R3OhZ4UZuJ8BlbQabFReu3Th6pZtGJwe12cOs4I3h1Gm_1bRuJidShPcOxX-AdyPkxQ</recordid><startdate>20060301</startdate><enddate>20060301</enddate><creator>Ma, J.</creator><creator>Weisberg, A.</creator><creator>Griffin, J.P.</creator><creator>Vaughan, D.E.</creator><creator>Fogo, A.B.</creator><creator>Brown, N.J.</creator><general>Elsevier Inc</general><general>Nature Publishing</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20060301</creationdate><title>Plasminogen activator inhibitor-1 deficiency protects against aldosterone-induced glomerular injury</title><author>Ma, J. ; Weisberg, A. ; Griffin, J.P. ; Vaughan, D.E. ; Fogo, A.B. ; Brown, N.J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c501t-3e5dca9302835bf183854bf3a63283759dc6a1b0ff3c2bb2e9d0369e0915a69f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Albuminuria - urine</topic><topic>aldosterone</topic><topic>Aldosterone - adverse effects</topic><topic>Aldosterone - pharmacology</topic><topic>angiotensin</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - drug effects</topic><topic>Blood Pressure - physiology</topic><topic>Chemokine CCL2 - analysis</topic><topic>Chemokine CCL2 - genetics</topic><topic>Collagen - analysis</topic><topic>Collagen - genetics</topic><topic>Fibronectins - analysis</topic><topic>Fibronectins - genetics</topic><topic>Gene Expression</topic><topic>Glomerulonephritis</topic><topic>Glomerulonephritis - chemically induced</topic><topic>Glomerulonephritis - physiopathology</topic><topic>Glomerulonephritis - prevention & control</topic><topic>Glomerulonephritis - urine</topic><topic>Hemodynamics - physiology</topic><topic>Kidney Glomerulus - chemistry</topic><topic>Kidney Glomerulus - drug effects</topic><topic>Kidney Glomerulus - pathology</topic><topic>Kidney Glomerulus - physiopathology</topic><topic>Macrophages - pathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Inbred Strains</topic><topic>Myocardium - chemistry</topic><topic>Myocardium - pathology</topic><topic>Nephrectomy</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><topic>Osteopontin</topic><topic>Plasminogen Activator Inhibitor 1 - deficiency</topic><topic>Plasminogen Activator Inhibitor 1 - genetics</topic><topic>Plasminogen Activator Inhibitor 1 - physiology</topic><topic>plasminogen activator inhibitor-1</topic><topic>RNA, Messenger - analysis</topic><topic>Sialoglycoproteins - analysis</topic><topic>Sialoglycoproteins - genetics</topic><topic>Sodium - urine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ma, J.</creatorcontrib><creatorcontrib>Weisberg, A.</creatorcontrib><creatorcontrib>Griffin, J.P.</creatorcontrib><creatorcontrib>Vaughan, D.E.</creatorcontrib><creatorcontrib>Fogo, A.B.</creatorcontrib><creatorcontrib>Brown, N.J.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ma, J.</au><au>Weisberg, A.</au><au>Griffin, J.P.</au><au>Vaughan, D.E.</au><au>Fogo, A.B.</au><au>Brown, N.J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Plasminogen activator inhibitor-1 deficiency protects against aldosterone-induced glomerular injury</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>2006-03-01</date><risdate>2006</risdate><volume>69</volume><issue>6</issue><spage>1064</spage><epage>1072</epage><pages>1064-1072</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract>This study tests the hypothesis that plasminogen activator inhibitor-1 (PAI-1) contributes to aldosterone-induced renal and cardiac injury. The effects of 12-week aldosterone (2.8 μg/day)/salt (1% drinking water) versus vehicle/salt on renal and cardiac histology and mRNA expression were determined in wild-type (WT) and PAI-1 deficient (PAI-1(−/−)) mice. Systolic blood pressure was similar in aldosterone-infused WT and PAI-1(−/−) mice until 12 weeks, when it was significantly higher in the WT mice. At 12 weeks, urine volume, sodium excretion, and sodium/potassium ratio were similarly increased in the two aldosterone-infused groups. In contrast, urine albumin excretion was greater in aldosterone-infused WT mice (mean±s.d.: 699.0±873.0 μg/24 h) compared to vehicle-infused WT (23.6±9.0 μg/24 h, P=0.003) or aldosterone-infused PAI-1(−/−) mice (131.6±110.6 μg/24 h, P=0.007). Aldosterone increased glomerular area to a greater extent in WT (4651±577 versus 3278±488 μm2/glomerulus in vehicle-infused WT, P<0.001) than in PAI-1(−/−) mice (3713±705 μm2/glomerulus, P=0.001 versus aldosterone-infused WT), with corresponding mesangial expansion. Renal collagen content was also increased in aldosterone-infused WT versus PAI-1(−/−) mice. In WT mice, aldosterone increased renal mRNA expression of PAI-1, collagen I, collagen III, osteopontin, fibronectin, monocyte chemoattractant protein-1 (MCP-1), and F4/80 (all P<0.05), but not transforming growth factor beta (TGF-β). In PAI-1(−/−) mice, aldosterone increased renal expression of collagen I, osteopontin, fibronectin, and MCP-1, and tended to increase collagen III. Renal osteopontin expression was diminished in aldosterone-treated PAI-1(−/−) compared to aldosterone-treated WT mice (P=0.05). Aldosterone induced cardiac hypertrophy but not fibrosis in WT and PAI-1(−/−) mice. PAI-1 contributes to aldosterone-induced glomerular injury.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>16528256</pmid><doi>10.1038/sj.ki.5000201</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Albuminuria - urine aldosterone Aldosterone - adverse effects Aldosterone - pharmacology angiotensin Animals Biological and medical sciences Blood Pressure - drug effects Blood Pressure - physiology Chemokine CCL2 - analysis Chemokine CCL2 - genetics Collagen - analysis Collagen - genetics Fibronectins - analysis Fibronectins - genetics Gene Expression Glomerulonephritis Glomerulonephritis - chemically induced Glomerulonephritis - physiopathology Glomerulonephritis - prevention & control Glomerulonephritis - urine Hemodynamics - physiology Kidney Glomerulus - chemistry Kidney Glomerulus - drug effects Kidney Glomerulus - pathology Kidney Glomerulus - physiopathology Macrophages - pathology Male Medical sciences Mice Mice, Inbred C57BL Mice, Inbred Strains Myocardium - chemistry Myocardium - pathology Nephrectomy Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure Osteopontin Plasminogen Activator Inhibitor 1 - deficiency Plasminogen Activator Inhibitor 1 - genetics Plasminogen Activator Inhibitor 1 - physiology plasminogen activator inhibitor-1 RNA, Messenger - analysis Sialoglycoproteins - analysis Sialoglycoproteins - genetics Sodium - urine |
| title | Plasminogen activator inhibitor-1 deficiency protects against aldosterone-induced glomerular injury |
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