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Angiotensin II Type II Receptor Deficiency Accelerates the Development of Nephropathy in Type I Diabetes via Oxidative Stress and ACE2
Joint Authors
Chen, Yun-Wen
Zhang, Shao-Ling
Chang, Shiao-Ying
Chenier, Isabelle
Tran, Stella Le Minh
Source
Issue
Vol. 2011, Issue 2011 (31 Dec. 2011), pp.1-12, 12 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2011-07-27
Country of Publication
Egypt
No. of Pages
12
Main Subjects
Abstract EN
Since the functional role(s) of angiotensin II (Ang II) type II receptor (AT2R) in type I diabetes is unknown, we hypothesized that AT2R is involved in decreasing the effects of type I diabetes on the kidneys.
We induced diabetes with low-dose streptozotocin (STZ) in both AT2R knockout (AT2RKO) and wild-type (WT) male mice aged 12 weeks and followed them for 4 weeks.
Three subgroups nondiabetic, diabetic, and insulin-treated diabetic (Rx insulin implant) were studied.
Systolic blood pressure (SBP), physiological parameters, glomerular filtration rate (GFR), renal morphology, gene expression, and apoptosis were assessed.
After 4 weeks of diabetes, compared to WT controls, AT2RKO mice clearly developed features of early diabetic nephropathy (DN), such as renal hypertrophy, tubular apoptosis, and progressive extracellular matrix (ECM) protein accumulation as well as increased GFR.
AT2RKO mice presented hypertension unaffected by diabetes.
Renal oxidative stress (measured as heme oxygenase 1 (HO-1) gene expression and reactive oxygen species (ROS) generation) and intrarenal renin angiotensin system components, such as angiotensinogen (Agt), AT1R, and angiotensin-converting enzyme (ACE) gene expression, were augmented whereas angiotensin-converting enzyme2 (ACE2) gene expression was decreased in renal proximal tubules (RPTs) of AT2RKO mice.
The renal changes noted above were significantly enhanced in diabetic AT2RKO mice but partially attenuated in insulin-treated diabetic WT and AT2RKO mice.
In conclusion, AT2R deficiency accelerates the development of DN, which appears to be mediated, at least in part, via heightened oxidative stress and ACE/ACE2 ratio in RPTs.
American Psychological Association (APA)
Chang, Shiao-Ying& Chen, Yun-Wen& Chenier, Isabelle& Tran, Stella Le Minh& Zhang, Shao-Ling. 2011. Angiotensin II Type II Receptor Deficiency Accelerates the Development of Nephropathy in Type I Diabetes via Oxidative Stress and ACE2. Journal of Diabetes Research،Vol. 2011, no. 2011, pp.1-12.
https://search.emarefa.net/detail/BIM-990643
Modern Language Association (MLA)
Chang, Shiao-Ying…[et al.]. Angiotensin II Type II Receptor Deficiency Accelerates the Development of Nephropathy in Type I Diabetes via Oxidative Stress and ACE2. Journal of Diabetes Research No. 2011 (2011), pp.1-12.
https://search.emarefa.net/detail/BIM-990643
American Medical Association (AMA)
Chang, Shiao-Ying& Chen, Yun-Wen& Chenier, Isabelle& Tran, Stella Le Minh& Zhang, Shao-Ling. Angiotensin II Type II Receptor Deficiency Accelerates the Development of Nephropathy in Type I Diabetes via Oxidative Stress and ACE2. Journal of Diabetes Research. 2011. Vol. 2011, no. 2011, pp.1-12.
https://search.emarefa.net/detail/BIM-990643
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-990643