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The Effect of ACE Inhibitors on The Gene Expression of TGF-R and TNF=a in Renal Tissues from Patients with IgA Nephropathy

Other Title
IgA 신증 환자들에서 신조직내GF-β와 TNF-α의 유전자발현에 대한 ACE Ihibitor의 영향
Kim, SJ; Shin, GT; Ma, KA; Kim, HS; Kim, DH
Taehan Sinjang Hakhoe chi, 19(4):604-611, 2000
Journal Title
Taehan Sinjang Hakhoe chi; The Korean journal of nephrology; 대한신장학회지
Progressive nephropathies are characterized by the enhanced accumulation of extracellular matrix in the kidney. Overproduction of transforming growth factor .8 (TGF- l3) was shown to result in pathological fibrosis of tissue via the accumulation of extracellular matrix proteins. It has been proposed that angiotensin 11 stimulates the production of TGF-.8. Despite accumulating volume of data supporting the effects of angiotensin converting enzyme (ACE) inhibitors in the attenuation of TGF-18 in vitro and in rats, studies . in humans are absolutely lacking. There is ´evidence that TNF- a expression is increased in various glomerulonephritis. The present study sought to determine the effects of ACE inhibitors on TGF- .8 1 and TNF- a in patients with IgA nephropathy. Using competitive polymerase chain reaction, TGF- R 1 and TNFa mRNA abundance were measured. Patients taking ACE inhibitors showed significantly lower renal TGF.81 gene expression compared with patients not on these medications (ratios of TGF-.81/Q-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 (427±0.62 versus 2.78±0.71). ACE inhibitor therapy did not affect the TNF- a mRNA expression in renal tissue. In conclusion, we observed a significant reduction of the TGF-Q 1 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.
Angioterlsin llACE inhibitorTGF- β
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Journal Papers > School of Medicine / Graduate School of Medicine > Nephrology
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