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| IgA 신증 환자들에서 신조직내 TGF-β와 TNF-α의 유전자발현에 대한 ACE Inhibitor의 영향 (The Effect of ACE Inhibitors on The Gene Expression of TGF-β and TNF- α in Renal Tissues from Patients with IgA Nephropathy) |
| 김승정(Seung Jung Kim),신규태(Gyu Tae Shin),마경애(Gyung Ae Ma),김홍수(Hong Soo Kim),김도현(Do Hyun Kim) |
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| Abstract |
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Progressive nephropathies are characterized by the enhanced accmulation of extracellular matrix in the kidney. Overproduction of transforming growth factor-β(TGF-β) 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-β. Despite accumulating volume of data supporting the effects of angiotensin converting enzyme(ACE) inhibitors in the attenuation of TGF-β in vitro and in rats, studies in humans are absolutely lacking. There is evidence that TNF-α expression is increased in various glomerulonephritis. The present study sought to determine the effects of ACE inhibitors on TGF-β1 and TNF-α in patients with IgA nephropathy. Using competitive polymerase chain reaction, TGF-β1 and TNF-α mRNA abundance were measured. Patients taking ACE inhibitors showed significantly lower renal TGF-β1 gene expression compared with paticnts not on these medications(ratios of TGF-β1/β-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-α mRNA expression in renal tissue. In conclusion, we observed a significant reduction of the TGF-β1 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. |
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