Delivery of Recombinant Adeno-Associated Virus-Mediated Human Tissue Kallikrein for Therapy of Chronic Renal Failure in Rats
The tissue kallikrein-kinin system is important in regulating cardiovascular and renal function, and dysregulation of the system has been implicated in heart and kidney pathologies. These findings suggest that if balance can be restored to the kallikrein-kinin axis, then associated disease progressi...
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| Veröffentlicht in: | Human gene therapy 2008-04, Vol.19 (4), p.318-330 |
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| creator | LING TU XIZHEN XU ZELDIN, Darryl C DAO WEN WANG HUAIBING WAN CHANGQING ZHOU JUANJUAN DENG GANG XU XIAO XIAO YIPU CHEN EDIN, Matthew L VOLTZ, James W |
| description | The tissue kallikrein-kinin system is important in regulating cardiovascular and renal function, and dysregulation of the system has been implicated in heart and kidney pathologies. These findings suggest that if balance can be restored to the kallikrein-kinin axis, then associated disease progression may be attenuated. To test this hypothesis, recombinant adeno-associated virus (rAAV)-mediated human tissue kallikrein (HK) expression was induced in a rodent model of chronic renal failure involving 5/6 nephrectomy (nephrectomy plus 70% reduction of remaining kidney). rAAV-HK treatment attenuated the rise in blood pressure, glomerular sclerosis, and tubulointerstitial injury observed in this model. rAAV-HK treatment also attenuated renal function decline as measured by urinary microalbumin, osmolarity, and cGMP levels. Reverse transcriptase-polymerase chain reaction analysis showed that rAAV-HK-treated rats had higher levels of bradykinin receptor-2 (B(2)R) and dopamine receptor-1 mRNAs. In contrast, angiotensin II receptor-1, endothelin receptor-A, and vasopressin receptor-2 mRNAs were markedly downregulated in kidneys from HK-treated rats. Bradykinin induced similar changes in receptor levels and prevented transforming growth factor-beta(1)-induced tubulointerstitial fibrosis. The effects of bradykinin could be reversed with the B(2)R antagonist HOE-140. Together, these findings suggest that restoration of the kallikrein-kinin system reduces kidney injury and protects renal function in 5/6-nephrectomized rats via changes in the expression and activation of G protein-coupled receptors including B(2)R. |
| doi_str_mv | 10.1089/hum.2007.138 |
| format | Article |
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These findings suggest that if balance can be restored to the kallikrein-kinin axis, then associated disease progression may be attenuated. To test this hypothesis, recombinant adeno-associated virus (rAAV)-mediated human tissue kallikrein (HK) expression was induced in a rodent model of chronic renal failure involving 5/6 nephrectomy (nephrectomy plus 70% reduction of remaining kidney). rAAV-HK treatment attenuated the rise in blood pressure, glomerular sclerosis, and tubulointerstitial injury observed in this model. rAAV-HK treatment also attenuated renal function decline as measured by urinary microalbumin, osmolarity, and cGMP levels. Reverse transcriptase-polymerase chain reaction analysis showed that rAAV-HK-treated rats had higher levels of bradykinin receptor-2 (B(2)R) and dopamine receptor-1 mRNAs. In contrast, angiotensin II receptor-1, endothelin receptor-A, and vasopressin receptor-2 mRNAs were markedly downregulated in kidneys from HK-treated rats. Bradykinin induced similar changes in receptor levels and prevented transforming growth factor-beta(1)-induced tubulointerstitial fibrosis. The effects of bradykinin could be reversed with the B(2)R antagonist HOE-140. Together, these findings suggest that restoration of the kallikrein-kinin system reduces kidney injury and protects renal function in 5/6-nephrectomized rats via changes in the expression and activation of G protein-coupled receptors including B(2)R.</description><identifier>ISSN: 1043-0342</identifier><identifier>EISSN: 1557-7422</identifier><identifier>DOI: 10.1089/hum.2007.138</identifier><identifier>PMID: 18402547</identifier><identifier>CODEN: HGTHE3</identifier><language>eng</language><publisher>Larchmont, NY: Liebert</publisher><subject>Albuminuria ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Applied cell therapy and gene therapy ; Biological and medical sciences ; Biotechnology ; Blood Pressure ; Bradykinin - pharmacology ; Chronic kidney failure ; Creatinine - blood ; Cyclic GMP - urine ; Dependovirus - genetics ; Dosage and administration ; Drug therapy ; Fundamental and applied biological sciences. Psychology ; Gene therapy ; Genetic Therapy ; Health aspects ; Health. Pharmaceutical industry ; Humans ; Industrial applications and implications. Economical aspects ; Kallikrein ; Kidney - metabolism ; Kidney - pathology ; Kidney Failure, Chronic - genetics ; Kidney Failure, Chronic - therapy ; Male ; Medical sciences ; Models, Animal ; Nephrectomy ; Phosphatidylinositol 3-Kinases - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; Rats ; Rats, Wistar ; Recombinant Proteins - administration & dosage ; Recombinant Proteins - genetics ; Recombinant Proteins - therapeutic use ; Risk factors ; Signal Transduction ; Tissue Kallikreins - administration & dosage ; Tissue Kallikreins - genetics ; Tissue Kallikreins - therapeutic use ; Transforming Growth Factor beta1 - pharmacology ; Transfusions. Complications. Transfusion reactions. Cell and gene therapy</subject><ispartof>Human gene therapy, 2008-04, Vol.19 (4), p.318-330</ispartof><rights>2008 INIST-CNRS</rights><rights>COPYRIGHT 2008 Mary Ann Liebert, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c479t-8ef351a325e94c0ab0bfb4bbe0991d8ad7dfaf17f213a51c80048475e2a7becf3</citedby><cites>FETCH-LOGICAL-c479t-8ef351a325e94c0ab0bfb4bbe0991d8ad7dfaf17f213a51c80048475e2a7becf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20316632$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18402547$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>LING TU</creatorcontrib><creatorcontrib>XIZHEN XU</creatorcontrib><creatorcontrib>ZELDIN, Darryl C</creatorcontrib><creatorcontrib>DAO WEN WANG</creatorcontrib><creatorcontrib>HUAIBING WAN</creatorcontrib><creatorcontrib>CHANGQING ZHOU</creatorcontrib><creatorcontrib>JUANJUAN DENG</creatorcontrib><creatorcontrib>GANG XU</creatorcontrib><creatorcontrib>XIAO XIAO</creatorcontrib><creatorcontrib>YIPU CHEN</creatorcontrib><creatorcontrib>EDIN, Matthew L</creatorcontrib><creatorcontrib>VOLTZ, James W</creatorcontrib><title>Delivery of Recombinant Adeno-Associated Virus-Mediated Human Tissue Kallikrein for Therapy of Chronic Renal Failure in Rats</title><title>Human gene therapy</title><addtitle>Hum Gene Ther</addtitle><description>The tissue kallikrein-kinin system is important in regulating cardiovascular and renal function, and dysregulation of the system has been implicated in heart and kidney pathologies. These findings suggest that if balance can be restored to the kallikrein-kinin axis, then associated disease progression may be attenuated. To test this hypothesis, recombinant adeno-associated virus (rAAV)-mediated human tissue kallikrein (HK) expression was induced in a rodent model of chronic renal failure involving 5/6 nephrectomy (nephrectomy plus 70% reduction of remaining kidney). rAAV-HK treatment attenuated the rise in blood pressure, glomerular sclerosis, and tubulointerstitial injury observed in this model. rAAV-HK treatment also attenuated renal function decline as measured by urinary microalbumin, osmolarity, and cGMP levels. Reverse transcriptase-polymerase chain reaction analysis showed that rAAV-HK-treated rats had higher levels of bradykinin receptor-2 (B(2)R) and dopamine receptor-1 mRNAs. In contrast, angiotensin II receptor-1, endothelin receptor-A, and vasopressin receptor-2 mRNAs were markedly downregulated in kidneys from HK-treated rats. Bradykinin induced similar changes in receptor levels and prevented transforming growth factor-beta(1)-induced tubulointerstitial fibrosis. The effects of bradykinin could be reversed with the B(2)R antagonist HOE-140. Together, these findings suggest that restoration of the kallikrein-kinin system reduces kidney injury and protects renal function in 5/6-nephrectomized rats via changes in the expression and activation of G protein-coupled receptors including B(2)R.</description><subject>Albuminuria</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Applied cell therapy and gene therapy</subject><subject>Biological and medical sciences</subject><subject>Biotechnology</subject><subject>Blood Pressure</subject><subject>Bradykinin - pharmacology</subject><subject>Chronic kidney failure</subject><subject>Creatinine - blood</subject><subject>Cyclic GMP - urine</subject><subject>Dependovirus - genetics</subject><subject>Dosage and administration</subject><subject>Drug therapy</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene therapy</subject><subject>Genetic Therapy</subject><subject>Health aspects</subject><subject>Health. Pharmaceutical industry</subject><subject>Humans</subject><subject>Industrial applications and implications. Economical aspects</subject><subject>Kallikrein</subject><subject>Kidney - metabolism</subject><subject>Kidney - pathology</subject><subject>Kidney Failure, Chronic - genetics</subject><subject>Kidney Failure, Chronic - therapy</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Models, Animal</subject><subject>Nephrectomy</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Recombinant Proteins - administration & dosage</subject><subject>Recombinant Proteins - genetics</subject><subject>Recombinant Proteins - therapeutic use</subject><subject>Risk factors</subject><subject>Signal Transduction</subject><subject>Tissue Kallikreins - administration & dosage</subject><subject>Tissue Kallikreins - genetics</subject><subject>Tissue Kallikreins - therapeutic use</subject><subject>Transforming Growth Factor beta1 - pharmacology</subject><subject>Transfusions. Complications. Transfusion reactions. Cell and gene therapy</subject><issn>1043-0342</issn><issn>1557-7422</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkl1rFDEUhgdR7IfeeS0DolfOms_JzE1hWa0VK0JZvQ1nMifd6EyyJjOFQn-8WXepFiQXyUme85CQtyheULKgpGnfbeZxwQhRC8qbR8UxlVJVSjD2OK-J4BXhgh0VJyn9IIRyWaunxRFtBGFSqOPi7j0O7gbjbRlseYUmjJ3z4Kdy2aMP1TKlYBxM2JffXZxT9QX7fXkxj-DLtUtpxvIzDIP7GdH50oZYrjcYYftHudrE4J3Jag9DeQ5umCOWmbuCKT0rnlgYEj4_zKfFt_MP69VFdfn146fV8rIyQrVT1aDlkgJnElthCHSks53oOiRtS_sGetVbsFRZRjlIahpCRCOURAaqQ2P5aXG2927nbsTeoJ8iDHob3QjxVgdw-uGJdxt9HW4046pmUmbBm4Mghl8zpkmPLhkcBvAY5qTrlgpJZZ3BV3vwGgbUztuQfWYH6yVVbd1KzkWmFv-h8uhxdCZ4tC7vP2h4u28wMaQU0d7fnRK9S4HOKdC7FOicgoy__Pe9f-HDt2fg9QGAZGCwEbxx6Z5jhNO65oz_Bjp_vCE</recordid><startdate>20080401</startdate><enddate>20080401</enddate><creator>LING TU</creator><creator>XIZHEN XU</creator><creator>ZELDIN, Darryl C</creator><creator>DAO WEN WANG</creator><creator>HUAIBING WAN</creator><creator>CHANGQING ZHOU</creator><creator>JUANJUAN DENG</creator><creator>GANG XU</creator><creator>XIAO XIAO</creator><creator>YIPU CHEN</creator><creator>EDIN, Matthew L</creator><creator>VOLTZ, James W</creator><general>Liebert</general><general>Mary Ann Liebert, Inc</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20080401</creationdate><title>Delivery of Recombinant Adeno-Associated Virus-Mediated Human Tissue Kallikrein for Therapy of Chronic Renal Failure in Rats</title><author>LING TU ; XIZHEN XU ; ZELDIN, Darryl C ; DAO WEN WANG ; HUAIBING WAN ; CHANGQING ZHOU ; JUANJUAN DENG ; GANG XU ; XIAO XIAO ; YIPU CHEN ; EDIN, Matthew L ; VOLTZ, James W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c479t-8ef351a325e94c0ab0bfb4bbe0991d8ad7dfaf17f213a51c80048475e2a7becf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Albuminuria</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>Applied cell therapy and gene therapy</topic><topic>Biological and medical sciences</topic><topic>Biotechnology</topic><topic>Blood Pressure</topic><topic>Bradykinin - pharmacology</topic><topic>Chronic kidney failure</topic><topic>Creatinine - blood</topic><topic>Cyclic GMP - urine</topic><topic>Dependovirus - genetics</topic><topic>Dosage and administration</topic><topic>Drug therapy</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene therapy</topic><topic>Genetic Therapy</topic><topic>Health aspects</topic><topic>Health. Pharmaceutical industry</topic><topic>Humans</topic><topic>Industrial applications and implications. Economical aspects</topic><topic>Kallikrein</topic><topic>Kidney - metabolism</topic><topic>Kidney - pathology</topic><topic>Kidney Failure, Chronic - genetics</topic><topic>Kidney Failure, Chronic - therapy</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Models, Animal</topic><topic>Nephrectomy</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Recombinant Proteins - administration & dosage</topic><topic>Recombinant Proteins - genetics</topic><topic>Recombinant Proteins - therapeutic use</topic><topic>Risk factors</topic><topic>Signal Transduction</topic><topic>Tissue Kallikreins - administration & dosage</topic><topic>Tissue Kallikreins - genetics</topic><topic>Tissue Kallikreins - therapeutic use</topic><topic>Transforming Growth Factor beta1 - pharmacology</topic><topic>Transfusions. Complications. Transfusion reactions. Cell and gene therapy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>LING TU</creatorcontrib><creatorcontrib>XIZHEN XU</creatorcontrib><creatorcontrib>ZELDIN, Darryl C</creatorcontrib><creatorcontrib>DAO WEN WANG</creatorcontrib><creatorcontrib>HUAIBING WAN</creatorcontrib><creatorcontrib>CHANGQING ZHOU</creatorcontrib><creatorcontrib>JUANJUAN DENG</creatorcontrib><creatorcontrib>GANG XU</creatorcontrib><creatorcontrib>XIAO XIAO</creatorcontrib><creatorcontrib>YIPU CHEN</creatorcontrib><creatorcontrib>EDIN, Matthew L</creatorcontrib><creatorcontrib>VOLTZ, James W</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Human gene therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>LING TU</au><au>XIZHEN XU</au><au>ZELDIN, Darryl C</au><au>DAO WEN WANG</au><au>HUAIBING WAN</au><au>CHANGQING ZHOU</au><au>JUANJUAN DENG</au><au>GANG XU</au><au>XIAO XIAO</au><au>YIPU CHEN</au><au>EDIN, Matthew L</au><au>VOLTZ, James W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Delivery of Recombinant Adeno-Associated Virus-Mediated Human Tissue Kallikrein for Therapy of Chronic Renal Failure in Rats</atitle><jtitle>Human gene therapy</jtitle><addtitle>Hum Gene Ther</addtitle><date>2008-04-01</date><risdate>2008</risdate><volume>19</volume><issue>4</issue><spage>318</spage><epage>330</epage><pages>318-330</pages><issn>1043-0342</issn><eissn>1557-7422</eissn><coden>HGTHE3</coden><abstract>The tissue kallikrein-kinin system is important in regulating cardiovascular and renal function, and dysregulation of the system has been implicated in heart and kidney pathologies. These findings suggest that if balance can be restored to the kallikrein-kinin axis, then associated disease progression may be attenuated. To test this hypothesis, recombinant adeno-associated virus (rAAV)-mediated human tissue kallikrein (HK) expression was induced in a rodent model of chronic renal failure involving 5/6 nephrectomy (nephrectomy plus 70% reduction of remaining kidney). rAAV-HK treatment attenuated the rise in blood pressure, glomerular sclerosis, and tubulointerstitial injury observed in this model. rAAV-HK treatment also attenuated renal function decline as measured by urinary microalbumin, osmolarity, and cGMP levels. Reverse transcriptase-polymerase chain reaction analysis showed that rAAV-HK-treated rats had higher levels of bradykinin receptor-2 (B(2)R) and dopamine receptor-1 mRNAs. In contrast, angiotensin II receptor-1, endothelin receptor-A, and vasopressin receptor-2 mRNAs were markedly downregulated in kidneys from HK-treated rats. Bradykinin induced similar changes in receptor levels and prevented transforming growth factor-beta(1)-induced tubulointerstitial fibrosis. The effects of bradykinin could be reversed with the B(2)R antagonist HOE-140. Together, these findings suggest that restoration of the kallikrein-kinin system reduces kidney injury and protects renal function in 5/6-nephrectomized rats via changes in the expression and activation of G protein-coupled receptors including B(2)R.</abstract><cop>Larchmont, NY</cop><pub>Liebert</pub><pmid>18402547</pmid><doi>10.1089/hum.2007.138</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Human gene therapy, 2008-04, Vol.19 (4), p.318-330 |
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| language | eng |
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| subjects | Albuminuria Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Applied cell therapy and gene therapy Biological and medical sciences Biotechnology Blood Pressure Bradykinin - pharmacology Chronic kidney failure Creatinine - blood Cyclic GMP - urine Dependovirus - genetics Dosage and administration Drug therapy Fundamental and applied biological sciences. Psychology Gene therapy Genetic Therapy Health aspects Health. Pharmaceutical industry Humans Industrial applications and implications. Economical aspects Kallikrein Kidney - metabolism Kidney - pathology Kidney Failure, Chronic - genetics Kidney Failure, Chronic - therapy Male Medical sciences Models, Animal Nephrectomy Phosphatidylinositol 3-Kinases - metabolism Proto-Oncogene Proteins c-akt - metabolism Rats Rats, Wistar Recombinant Proteins - administration & dosage Recombinant Proteins - genetics Recombinant Proteins - therapeutic use Risk factors Signal Transduction Tissue Kallikreins - administration & dosage Tissue Kallikreins - genetics Tissue Kallikreins - therapeutic use Transforming Growth Factor beta1 - pharmacology Transfusions. Complications. Transfusion reactions. Cell and gene therapy |
| title | Delivery of Recombinant Adeno-Associated Virus-Mediated Human Tissue Kallikrein for Therapy of Chronic Renal Failure in Rats |
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