Matches in SemOpenAlex for { <https://semopenalex.org/work/W2000855130> ?p ?o ?g. }
- W2000855130 endingPage "1260" @default.
- W2000855130 startingPage "1250" @default.
- W2000855130 abstract "Adenovirus-mediated kallikrein gene delivery reverses salt-induced renal injury in Dahl salt-sensitive rats.BackgroundThe tissue kallikrein-kinin system has been shown to play a role in cardiac and renal functions. In this study, we investigated the ability of kallikrein gene delivery to reverse salt-induced cardiac hypertrophy and renal injury in Dahl salt-sensitive rats.MethodsAdenovirus harboring the human tissue kallikrein gene, Ad.CMV-cHK, was delivered intravenously into Dahl salt-sensitive rats suffering from hypertension, cardiac hypertrophy and renal damage induced by a high salt diet (4% NaCl) for four weeks.ResultsExpression of human kallikrein mRNA was detected in rat kidney, heart, aorta and liver, and immunoreactive human kallikrein levels were measured in the serum and urine of rats receiving gene delivery. A single injection of Ad.CMV-cHK caused a significant reduction of blood pressure for more than two weeks. Kallikrein gene transfer caused left ventricular mass reduction and elevated glomerular filtration rate, renal blood flow, urinary excretion, urinary kinin, nitrite/nitrate content, cGMP and cAMP levels. Morphological investigations showed that kallikrein gene transfer caused a significant reversal in salt-induced tissue and organ damage. In the heart, cardiac hypertrophy and fibrosis were reduced, and in the kidney, both glomerular sclerotic lesions and tubular damage were reversed.ConclusionsAdenovirus-mediated kallikrein gene delivery is effective in reversing salt-induced cardiac hypertrophy and renal injury in Dahl-salt sensitive rats. Adenovirus-mediated kallikrein gene delivery reverses salt-induced renal injury in Dahl salt-sensitive rats. The tissue kallikrein-kinin system has been shown to play a role in cardiac and renal functions. In this study, we investigated the ability of kallikrein gene delivery to reverse salt-induced cardiac hypertrophy and renal injury in Dahl salt-sensitive rats. Adenovirus harboring the human tissue kallikrein gene, Ad.CMV-cHK, was delivered intravenously into Dahl salt-sensitive rats suffering from hypertension, cardiac hypertrophy and renal damage induced by a high salt diet (4% NaCl) for four weeks. Expression of human kallikrein mRNA was detected in rat kidney, heart, aorta and liver, and immunoreactive human kallikrein levels were measured in the serum and urine of rats receiving gene delivery. A single injection of Ad.CMV-cHK caused a significant reduction of blood pressure for more than two weeks. Kallikrein gene transfer caused left ventricular mass reduction and elevated glomerular filtration rate, renal blood flow, urinary excretion, urinary kinin, nitrite/nitrate content, cGMP and cAMP levels. Morphological investigations showed that kallikrein gene transfer caused a significant reversal in salt-induced tissue and organ damage. In the heart, cardiac hypertrophy and fibrosis were reduced, and in the kidney, both glomerular sclerotic lesions and tubular damage were reversed. Adenovirus-mediated kallikrein gene delivery is effective in reversing salt-induced cardiac hypertrophy and renal injury in Dahl-salt sensitive rats." @default.
- W2000855130 created "2016-06-24" @default.
- W2000855130 creator A5007067184 @default.
- W2000855130 creator A5058401832 @default.
- W2000855130 creator A5066893221 @default.
- W2000855130 creator A5091050446 @default.
- W2000855130 date "1998-10-01" @default.
- W2000855130 modified "2023-09-25" @default.
- W2000855130 title "Adenovirus-mediated kallikrein gene delivery reverses salt-induced renal injury in Dahl salt-sensitive rats" @default.
- W2000855130 cites W1489992640 @default.
- W2000855130 cites W183226119 @default.
- W2000855130 cites W1964315955 @default.
- W2000855130 cites W1966110783 @default.
- W2000855130 cites W1967644583 @default.
- W2000855130 cites W1977311294 @default.
- W2000855130 cites W1978068869 @default.
- W2000855130 cites W1984901440 @default.
- W2000855130 cites W1988644982 @default.
- W2000855130 cites W1989982905 @default.
- W2000855130 cites W1992529389 @default.
- W2000855130 cites W2009945363 @default.
- W2000855130 cites W2019114393 @default.
- W2000855130 cites W2020385191 @default.
- W2000855130 cites W2025540579 @default.
- W2000855130 cites W2031325309 @default.
- W2000855130 cites W2038438421 @default.
- W2000855130 cites W2053097440 @default.
- W2000855130 cites W2054466992 @default.
- W2000855130 cites W2060302745 @default.
- W2000855130 cites W2062427601 @default.
- W2000855130 cites W2063153711 @default.
- W2000855130 cites W2064602583 @default.
- W2000855130 cites W2074936523 @default.
- W2000855130 cites W2091697250 @default.
- W2000855130 cites W2098945680 @default.
- W2000855130 cites W2121924030 @default.
- W2000855130 cites W2132445863 @default.
- W2000855130 cites W2134003126 @default.
- W2000855130 cites W2136984465 @default.
- W2000855130 cites W2145603947 @default.
- W2000855130 cites W2150971385 @default.
- W2000855130 cites W2158259279 @default.
- W2000855130 cites W2167748776 @default.
- W2000855130 cites W2320655060 @default.
- W2000855130 cites W2417164004 @default.
- W2000855130 cites W4244507161 @default.
- W2000855130 doi "https://doi.org/10.1046/j.1523-1755.1998.00104.x" @default.
- W2000855130 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9767541" @default.
- W2000855130 hasPublicationYear "1998" @default.
- W2000855130 type Work @default.
- W2000855130 sameAs 2000855130 @default.
- W2000855130 citedByCount "47" @default.
- W2000855130 countsByYear W20008551302012 @default.
- W2000855130 countsByYear W20008551302013 @default.
- W2000855130 countsByYear W20008551302014 @default.
- W2000855130 countsByYear W20008551302015 @default.
- W2000855130 countsByYear W20008551302016 @default.
- W2000855130 countsByYear W20008551302017 @default.
- W2000855130 countsByYear W20008551302018 @default.
- W2000855130 crossrefType "journal-article" @default.
- W2000855130 hasAuthorship W2000855130A5007067184 @default.
- W2000855130 hasAuthorship W2000855130A5058401832 @default.
- W2000855130 hasAuthorship W2000855130A5066893221 @default.
- W2000855130 hasAuthorship W2000855130A5091050446 @default.
- W2000855130 hasBestOaLocation W20008551301 @default.
- W2000855130 hasConcept C126322002 @default.
- W2000855130 hasConcept C134018914 @default.
- W2000855130 hasConcept C152328610 @default.
- W2000855130 hasConcept C159641895 @default.
- W2000855130 hasConcept C167414201 @default.
- W2000855130 hasConcept C170493617 @default.
- W2000855130 hasConcept C181199279 @default.
- W2000855130 hasConcept C2776246183 @default.
- W2000855130 hasConcept C2779591629 @default.
- W2000855130 hasConcept C2780091579 @default.
- W2000855130 hasConcept C52853521 @default.
- W2000855130 hasConcept C55493867 @default.
- W2000855130 hasConcept C71924100 @default.
- W2000855130 hasConcept C86803240 @default.
- W2000855130 hasConceptScore W2000855130C126322002 @default.
- W2000855130 hasConceptScore W2000855130C134018914 @default.
- W2000855130 hasConceptScore W2000855130C152328610 @default.
- W2000855130 hasConceptScore W2000855130C159641895 @default.
- W2000855130 hasConceptScore W2000855130C167414201 @default.
- W2000855130 hasConceptScore W2000855130C170493617 @default.
- W2000855130 hasConceptScore W2000855130C181199279 @default.
- W2000855130 hasConceptScore W2000855130C2776246183 @default.
- W2000855130 hasConceptScore W2000855130C2779591629 @default.
- W2000855130 hasConceptScore W2000855130C2780091579 @default.
- W2000855130 hasConceptScore W2000855130C52853521 @default.
- W2000855130 hasConceptScore W2000855130C55493867 @default.
- W2000855130 hasConceptScore W2000855130C71924100 @default.
- W2000855130 hasConceptScore W2000855130C86803240 @default.
- W2000855130 hasIssue "4" @default.
- W2000855130 hasLocation W20008551301 @default.
- W2000855130 hasLocation W20008551302 @default.
- W2000855130 hasOpenAccess W2000855130 @default.
- W2000855130 hasPrimaryLocation W20008551301 @default.