کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8304759 | 1538413 | 2015 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Differential regulation of angiotensin converting enzyme 2 and nuclear factor-κB by angiotensin II receptor subtypes in type 2 diabetic kidney
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کلمات کلیدی
ACE2angiotensin II type-1 receptorNPDAT2RAT1RT2DSTZHFDRASSBPTBARSkeap1 - buy1NOx - NOXangiotensin converting enzyme 2 - آنژیوتانسین تبدیل آنزیم 2Angiotensin II - آنژیوتانسین دوstreptozotocin - استرپتوزوتوسینNADPH oxidase - اکسیداز NADPH Oxidative stress - تنش اکسیداتیوAng II - دومType 2 diabetes - دیابت نوع 2High fat diet - رژیم غذایی با چربی بالاRenin angiotensin system - سیستم آنژیوتانسین رینینsystolic blood pressure - فشار خون سیستولیکType 2 diabetic nephropathy - نفروپاتی دیابتی نوع 2AT1 receptor - گیرنده AT1AT2 receptor - گیرنده AT2
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Angiotensin II (Ang II) acts through Angiotensin Converting Enzyme (ACE)/Ang II type 1 receptor (AT1R) axis to promote renal failure whereas the Ang II type 2 receptor (AT2R)/Angiotensin Converting Enzyme 2 (ACE2)/Ang1-7/Mas axis constitutes the protective arm of Renin Angiotensin System (RAS). Though Ang II has been known to activate the Nuclear Factor-κB (NF-κB) signalling pathway through different receptor subtype(s) in different tissues under various diseases, the subtype orchestrating this stimulation in type 2 diabetic kidney remains elusive. ACE2, a protective monocarboxypeptidase, responsible for conversion of Ang II to Ang1-7, opposes the deleterious effects of RAS pathway but how its expression is altered with blockade of AT1R and AT2R is not yet known. Hence, the present study was conceived to understand the regulation of NF-κB and ACE2 by using specific AT1 and AT2 receptor antagonists in non-genetic model of type 2 diabetic nephropathy. Our results show that the AT1R and AT2R antagonists lead to the repression and activation of NF-κB signalling pathway, respectively which suggests the role of AT1R in NF-κB activation. The blockade of AT2R led to an increase in ACE2 expression, which may be a compensatory response to the drastically increased inflammatory mediators and oxidative stress in the diabetic kidney. To the best of our knowledge, this is the first study showing the differential regulation of NF-κB and ACE2 by Ang II receptor subtypes and thus this study improves our understanding regarding regulation of inflammatory cascade and ACE2 by AT1R and AT2R in type 2 diabetic kidney, which may help in designing novel strategies to combat the disease in future.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimie - Volume 118, November 2015, Pages 71-81
Journal: Biochimie - Volume 118, November 2015, Pages 71-81
نویسندگان
Anuradha Pandey, Santosh Kumar Goru, Almesh Kadakol, Vajir Malek, Anil Bhanudas Gaikwad,