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Attenuating effect of angiotensin-(1–7) on angiotensin II-mediated NAD(P)H oxidase activation in type 2 diabetic nephropathy of KK-Ay/Ta mice

Attenuating effect of angiotensin-(1–7) on angiotensin II-mediated NAD(P)H oxidase activation in... Abstract ANG-(1–7) is associated with vasodilation and nitric oxide synthase stimulation. However, the role of ANG-(1–7) in type 2 diabetes mellitus is unknown. In this study, we examined the hypothesis that ANG-(1–7) attenuates ANG II-induced reactive oxygen species stress (ROS)-mediated injury in type 2 diabetic nephropathy of KK-A y /Ta mice. KK-A y /Ta mice were divided into four groups: 1 ) a control group; 2 ) ANG II infusion group; 3 ) ANG II+ANG-(1–7) coinfusion group; and 4 ) ANG II+ANG-(1–7)+ d -Ala 7 -ANG-(1–7) (A779) coinfusion group. In addition, primary mesangial cells were cultured and then stimulated with 25 mM glucose with or without ANG II, ANG-(1–7), and A779. The ANG II+ANG-(1–7) coinfusion group showed a lower urinary albumin/creatinine ratio increase than the ANG II group. ANG-(1–7) attenuated ANG II-mediated NAD(P)H oxidase activation and ROS production in diabetic glomeruli and mesangial cells. ANG II-induced NF-κB and MAPK signaling activation was also attenuated by ANG-(1–7) in the mesangial cells. These findings were related to improved mesangial expansion and to fibronectin and transforming growth factor-β1 production in response to ANG II and suggest that ANG-(1–7) may attenuate ANG II-stimulated ROS-mediated injury in type 2 diabetic nephropathy. The ACE2-ANG-(1–7)-Mas receptor axis should be investigated as a novel target for treatment of type 2 diabetic nephropathy. Copyright © 2011 the American Physiological Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Renal Physiology The American Physiological Society

Attenuating effect of angiotensin-(1–7) on angiotensin II-mediated NAD(P)H oxidase activation in type 2 diabetic nephropathy of KK-Ay/Ta mice

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References (44)

Publisher
The American Physiological Society
Copyright
Copyright © 2011 the American Physiological Society
ISSN
0363-6127
eISSN
1522-1466
DOI
10.1152/ajprenal.00065.2010
pmid
21367916
Publisher site
See Article on Publisher Site

Abstract

Abstract ANG-(1–7) is associated with vasodilation and nitric oxide synthase stimulation. However, the role of ANG-(1–7) in type 2 diabetes mellitus is unknown. In this study, we examined the hypothesis that ANG-(1–7) attenuates ANG II-induced reactive oxygen species stress (ROS)-mediated injury in type 2 diabetic nephropathy of KK-A y /Ta mice. KK-A y /Ta mice were divided into four groups: 1 ) a control group; 2 ) ANG II infusion group; 3 ) ANG II+ANG-(1–7) coinfusion group; and 4 ) ANG II+ANG-(1–7)+ d -Ala 7 -ANG-(1–7) (A779) coinfusion group. In addition, primary mesangial cells were cultured and then stimulated with 25 mM glucose with or without ANG II, ANG-(1–7), and A779. The ANG II+ANG-(1–7) coinfusion group showed a lower urinary albumin/creatinine ratio increase than the ANG II group. ANG-(1–7) attenuated ANG II-mediated NAD(P)H oxidase activation and ROS production in diabetic glomeruli and mesangial cells. ANG II-induced NF-κB and MAPK signaling activation was also attenuated by ANG-(1–7) in the mesangial cells. These findings were related to improved mesangial expansion and to fibronectin and transforming growth factor-β1 production in response to ANG II and suggest that ANG-(1–7) may attenuate ANG II-stimulated ROS-mediated injury in type 2 diabetic nephropathy. The ACE2-ANG-(1–7)-Mas receptor axis should be investigated as a novel target for treatment of type 2 diabetic nephropathy. Copyright © 2011 the American Physiological Society

Journal

AJP - Renal PhysiologyThe American Physiological Society

Published: Jun 1, 2011

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