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

Authors
Shin, GT; Kim, SJ; Ma, KA; Kim, HS; Kim, D
Citation
American journal of kidney diseases : the official journal of the National Kidney Foundation, 36(5):894-902, 2000
Journal Title
American journal of kidney diseases : the official journal of the National Kidney Foundation
ISSN
0272-63861523-6838
Abstract
Progressive 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.
MeSH terms
AdolescentAdultAgedAmlodipine/pharmacologyAngiotensin-Converting Enzyme Inhibitors/*pharmacologyCalcium Channel Blockers/therapeutic useFemaleGene Expression RegulationGlomerulonephritis/blood/*drug therapy/urineGlomerulonephritis, IGA/blood/urineHumansKidney/*drug effects/metabolismMaleMiddle AgedNifedipine/pharmacologyPolymerase Chain Reaction/methodsRNA, Messenger/blood/urineTransforming Growth Factor beta/blood/*drug effects/urineTransforming Growth Factor beta1
PMID
11054345
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Nephrology
AJOU Authors
신, 규태김, 흥수김, 도헌
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