The Effect of ACE Inhibitors on The Gene Expression of TGF-beta and TNF-alpha in Renal Tissues from Patients with IgA Nephropathy.
- Author:
Seung Jung KIM
1
;
Gyu Tae SHIN
;
Kyoung Ai MA
;
Heung Soo KIM
;
Do Hun KIM
Author Information
1. Department of Nephrology, School of Medicine, Ajou University, Suwon, Korea.
- Publication Type:In Vitro ; Original Article
- Keywords:
Angiotensin II;
ACE inhibitor;
TGF-beta
- MeSH:
Angiotensin II;
Angiotensin-Converting Enzyme Inhibitors*;
Angiotensins;
Animals;
Extracellular Matrix;
Extracellular Matrix Proteins;
Fibrosis;
Gene Expression*;
Glomerulonephritis;
Glomerulonephritis, IGA*;
Humans;
Immunoglobulin A*;
Kidney;
Polymerase Chain Reaction;
Rats;
Renal Insufficiency, Chronic;
RNA, Messenger;
Transforming Growth Factor beta*;
Transforming Growth Factor beta1;
Tumor Necrosis Factor-alpha*
- From:Korean Journal of Nephrology
2000;19(4):604-611
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Progressive nephropathies are characterized by the enhanced accmulation of extracellular matrix in the kidney. Overproduction of transforming growth factor-beta(TGF-beta) was shown to result in pathological fibrosis of tissue via the accumulation of extracellular matrix proteins. It has been proposed that angiotensin II stimulates the production of TGF-beta. Despite accumulating volume of data supporting the effects of angiotensin converting enzyme(ACE) inhibitors in the attenuation of TGF-beta in vitro and in rats, studies in humans are absolutely lacking. There is evidence that TNF-alpha expression is increased in various glomerulonephritis. The present study sought to determine the effects of ACE inhibitors on TGF-beta1 and TNF-alpha in patients with IgA nephropathy. Using competitive polymerase chain reaction, TGF-beta1 and TNF-alpha mRNA abundance were measured. Patients taking ACE inhibitors showed significantly lower renal TGF-beta1 gene expression compared with patients not on these medications(ratios of TGF-beta1/beta-actin, 4.27+/-0.62 versus 14.81+/-3.87, p<0.05), whereas no difference was noted between patients on ACE inhibitors and normal controls(4.27+/-0.62 versus 2.78+/-0.71). ACE inhibitor therapy did not affect the TNF-alpha mRNA expres- sion in renal tissue. In conclusion, we observed a significant reduction of the 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.
