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Angiotensin II Type II Receptor Deficiency Accelerates the Development of Nephropathy in Type I Diabetes via Oxidative Stress and ACE2
المؤلفون المشاركون
Chen, Yun-Wen
Zhang, Shao-Ling
Chang, Shiao-Ying
Chenier, Isabelle
Tran, Stella Le Minh
المصدر
العدد
المجلد 2011، العدد 2011 (31 ديسمبر/كانون الأول 2011)، ص ص. 1-12، 12ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2011-07-27
دولة النشر
مصر
عدد الصفحات
12
التخصصات الرئيسية
الملخص 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.
نمط استشهاد جمعية علماء النفس الأمريكية (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
نمط استشهاد الجمعية الأمريكية للغات الحديثة (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
نمط استشهاد الجمعية الطبية الأمريكية (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
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-990643
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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