کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10738073 | 1046682 | 2011 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Generation and characterization of a novel kidney-specific manganese superoxide dismutase knockout mouse
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کلمات کلیدی
MnSODouter medullaCre-recombinaseTAL - ازPeriodic Acid Schiff - اسید فسفریکThick ascending limb - اندام صعودی ضخیمIHC - ایمونوهیستوشیمیImmunohistochemistry - ایمونوهیستوشیمیDistal tubule - تومور دیستالbase pair - جفت پایهSuperoxide - سوپر اکسیدmanganese superoxide dismutase - سوپر اکسید دیسموتاز منگنزBlood pressure - فشارخونCortex - قشرproximal tubule - لوله پروگزیمالInner medulla - مدول داخلیCopper, zinc superoxide dismutase - مس، سوپراکسید دیسموتاز رویknockout - ناکاوتPAS - نهwild type - نوع وحشیnitrotyrosine - نیتروتیروستینpolymerase chain reaction - واکنش زنجیره ای پلیمرازPCR - واکنش زنجیرهٔ پلیمرازCre recombinase - کرم recombinaseKidney - کلیه
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Inactivation of manganese superoxide dismutase (MnSOD), a mitochondrial antioxidant, has been associated with renal disorders and often results in detrimental downstream events that are mechanistically not clear. Development of an animal model that exhibits kidney-specific deficiency of MnSOD would be extremely beneficial in exploring the downstream events that occur following MnSOD inactivation. Using Cre-Lox recombination technology, kidney-specific MnSOD deficient mice (both 100% and 50%) were generated that exhibited low expression of MnSOD in discrete renal cell types and reduced enzymatic activity within the kidney. These kidney-specific 100% KO mice possessed a normal life-span, although it was interesting that the mice were smaller. Consistent with the important role in scavenging superoxide radicals, the kidney-specific KO mice showed a significant increase in oxidative stress (tyrosine nitration) in a gene-dose dependent manner. In addition, loss of MnSOD resulted in mild renal damage (tubular dilation and cell swelling). Hence, this novel mouse model will aid in determining the specific role (local and/or systemic) governed by MnSOD within certain kidney cells. Moreover, these mice will serve as a powerful tool to explore molecular mechanisms that occur downstream of MnSOD inactivation in renal disorders or possibly in other pathologies that rely on normal renal function.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 51, Issue 2, 15 July 2011, Pages 406-416
Journal: Free Radical Biology and Medicine - Volume 51, Issue 2, 15 July 2011, Pages 406-416
نویسندگان
Nirmala Parajuli, Akira Marine, Sloane Simmons, Hamida Saba, Tanecia Mitchell, Takahiko Shimizu, Takuji Shirasawa, Lee Ann MacMillan-Crow,