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논문분류	춘계학술대회 초록집
제목	Murine Recombinant ACE2 Attenuates Kidney Injury in Experimental Alport’s Syndrome
저자	Eun Hui Bae5, Ana Konvalinka2, Fei Fang2, Xiaohua Zhou1, Vanessa Williams1, John Tran1, Xuewen Song1, Shao-Ling Zhang4, Rohan John6, Gavin Y. Oudit3, York Pei7, James William Scholey4
출판정보	2015; 2015(1):
키워드	Alport, ACE2, RAS
초록	Background: ACE2 is a monocarboxypeptidase in the renin angiotensin system that catalyzes the breakdown of Angiotensin II (AngII) to Ang1-7. We have reported that ACE2 expression and activity in the kidney are reduced in experimental AS but the impact of this finding on kidney disease progression has not been studied. Methods: we evaluated the effects of treatment with murine recombinant ACE2 (mrACE2) in Col4A3-/- mice, a model of AS characterized by proteinuria and progressive renal injury. mrACE2 was administered from 4-7 weeks of age via osmotic mini-pump. Results: Treatment with mrACE2 led to an increase in both kidney renal ACE2 expression and the urinary ACE2 excretion rate in 7-week-old Col4A3-/- mice compared to untreated group. Kidney AngII levels declined and kidney Ang1-7 levels increased. These effects were associated with a significant decrease in proteinuria in the treated 7- week-old Col4A3-/- mice compared to the untreated group. Ang II infusion induced Tumor necrosis factor α (TNF-α) converting enzyme (TACE) expression and activity and decreased ACE2 expression and activity which were counter-regulated by mrACE2 treatment. The inflammatory cytokine IL-6 and F4/80, a macrophage marker, were also reduced by treatment with mrACE2. Transforming growth factor-β1 (TGF-β1), col1α1, and alpha smooth muscle actin levels were increased in the kidneys of 7-week-old Col4A3-/- mice and all were reduced by mrACE2. Conclusion: Treatment with mrACE2 alters angiotensin peptide metabolism in the kidneys of Col4A3-/- mice and attenuates the progression of AS nephropathy.
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