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논문분류	춘계학술대회 초록집
제목	Murine Recombinant ACE2 Reduces Renal Fibrosis in Experimental Alport Syndrome(AS)
저자	Eun Hui Bae,1,5Ana Konvalinka,2 Fei Fang,1 Xiaohua Zhou,1Vanessa Williams,1John Tran,1 Xuewen Song,4 Shao-Ling Zhang,6 Rohan John,3 Vaibhav Patel,7 Gavin Y. Oudit,7 York Pei,4 and James William Scholey1,2
출판정보	2016; 2016(1):
키워드	Alport syndrome, renin-angiotensin system, renal fibrosis, ACE2, TACE
초록	ACE2 is a monocarboxypeptidase in the renin angiotensin system that catalyzes the breakdown of angiotensin II (AngII) to angiotensin-(1-7) (Ang1-7). We have reported that ACE2 expression and activity in kidney are reduced in experimental Alport Syndrom (AS) but the impact of this finding on disease progression has not been studied. Accordingly, we evaluated the effects of murine recombinant ACE2 (mrACE2) treatment in Col4A3-/- mice, a model of AS characterized by proteinuria and progressive renal injury. mrACE2 (0.5mg/kg/day) was administered from 4 -7 weeks of age via osmotic mini-pump. Treatment with mrACE2 led to an increased urinary ACE2 excretion, reduced renal AngII level and a correspondingly increased Ang1-7 level in 7-week-old Col4A3-/- mice. Pathological structural changes and albuminuria in the mutant mice were both attenuated by mrACE2 administration. mrACE2 ameliorated kidney fibrosis in Col4A3-/- mice as shown by decreased expression of profibrotic genes, less accumulation of extracellular matrix proteins and inhibition of the TGF-β signaling activation. Further, the increases in proinflammatory cytokine expression, macrophage infiltration, inflammatory signaling pathway activation and heme oxygenase-1 (HO-1) level in Col4A3-/- mice were also reduced by mrACE2 treatment. Lastly, mrACE2 influenced the turnover of renal ACE2, as it suppressed the expression of TNF-α converting enzyme (TACE), a negative regulator of ACE2. In summary, treatment with mrACE2 alters angiotensin peptide metabolism in the kidneys of Col4A3-/- mice and attenuates the progression of AS nephropathy.
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