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ACE inhibitors attenuate expression of renal transforming growth factor-beta1 in humans.

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dc.contributor.authorShin, GT-
dc.contributor.authorKim, SJ-
dc.contributor.authorMa, KA-
dc.contributor.authorKim, HS-
dc.contributor.authorKim, D-
dc.date.accessioned2011-07-28T01:53:00Z-
dc.date.available2011-07-28T01:53:00Z-
dc.date.issued2000-
dc.identifier.issn0272-6386-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/3649-
dc.description.abstractProgressive nephropathies are characterized by the enhanced accumulation of extracellular matrix in the kidney. Overproduction of transforming growth factor-beta (TGF-beta) was shown to result in pathological tissue fibrosis through the accumulation of extracellular matrix proteins. It has been proposed that angiotensin II stimulates TGF-beta production. Despite accumulating data supporting the effects of angiotensin-converting enzyme (ACE) inhibitors on the attenuation of TGF-beta in vitro and in rats, such studies in humans are lacking. The present study sought to determine the effects of ACE inhibitors on TGF-beta1 in patients with glomerulonephritis. Using competitive polymerase chain reaction and the sandwich enzyme-linked immunosorbent assay, TGF-beta1 messenger RNA (mRNA) abundance and TGF-beta1 protein levels were measured. Patients with immunoglobulin A nephropathy administered ACE inhibitors showed significantly lower renal TGF-beta1 gene expression than patients not administered these medications (mean ratios of TGF-beta1/beta-actin, 4.27 +/- 0.62 [SEM] versus 14.81 +/- 3.87; P < 0.05), whereas no difference was noted between patients administered ACE inhibitors and healthy controls (4.27 +/- 0.62 versus 2.78 +/- 0.71). ACE inhibitor therapy did not affect TGF-beta1 mRNA expression in freshly isolated mononuclear cells. Urine and serum TGF-beta1 protein levels were not affected by the administration of ACE inhibitors. However, possibly a longer duration of treatment would decrease TGF-beta1 levels in urine or blood. In conclusion, we observed a significant reduction in TGF-beta1 expression in the kidney by ACE inhibitors, and this suggests that the effects of ACE inhibitors observed in animals can be extrapolated to patients with chronic renal disease.-
dc.language.isoen-
dc.subject.MESHAdolescent-
dc.subject.MESHAdult-
dc.subject.MESHAged-
dc.subject.MESHAmlodipine-
dc.subject.MESHAngiotensin-Converting Enzyme Inhibitors-
dc.subject.MESHCalcium Channel Blockers-
dc.subject.MESHFemale-
dc.subject.MESHGene Expression Regulation-
dc.subject.MESHGlomerulonephritis-
dc.subject.MESHGlomerulonephritis, IGA-
dc.subject.MESHHumans-
dc.subject.MESHKidney-
dc.subject.MESHMale-
dc.subject.MESHMiddle Aged-
dc.subject.MESHNifedipine-
dc.subject.MESHPolymerase Chain Reaction-
dc.subject.MESHRNA, Messenger-
dc.subject.MESHTransforming Growth Factor beta-
dc.subject.MESHTransforming Growth Factor beta1-
dc.titleACE inhibitors attenuate expression of renal transforming growth factor-beta1 in humans.-
dc.typeArticle-
dc.identifier.pmid11054345-
dc.contributor.affiliatedAuthor신, 규태-
dc.contributor.affiliatedAuthor김, 흥수-
dc.contributor.affiliatedAuthor김, 도헌-
dc.type.localJournal Papers-
dc.citation.titleAmerican journal of kidney diseases-
dc.citation.volume36-
dc.citation.number5-
dc.citation.date2000-
dc.citation.startPage894-
dc.citation.endPage902-
dc.identifier.bibliographicCitationAmerican journal of kidney diseases, 36(5). : 894-902, 2000-
dc.identifier.eissn1523-6838-
dc.relation.journalidJ002726386-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Nephrology
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