کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10815931 | 1058530 | 2015 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Hyperglycemia  enhances kidney cell injury in HIVAN through down-regulation of vitamin D receptors
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کلمات کلیدی
global glomerulosclerosisGGSCGS8-OHdGHIVANVDRHAARTFSGS8-hydroxydeoxyguanosine - 8 هیدروکسی دیواکسی گوآزینKidney injury - آسیب کلیهDNA damage - آسیبDNAOxidative stress - تنش اکسیداتیوBUN - خوبHighly active anti-retroviral therapy - درمان ضد رتروویروسی بسیار فعالdihydroethidium - دی هیدروتیدیمDiabetic nephropathy - نفروپاتی دیابتیHIV-associated nephropathy - نفروپاتی وابسته به HIVblood urea nitrogen - نیتروژن اوره خونAGT - هشتDHE - وFocal segmental glomerulosclerosis - گلومرول اسکلروز بخش مرکزی فوکوسVitamin D receptor - گیرنده ویتامین D
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
In the present study, we evaluated the effect of short term hyperglycemia on renal lesions in a mouse model (Tg26) of HIV-associated nephropathy (HIVAN). Control and Tg26 mice in groups (n = 6) were administered either normal saline (FVBN or Tg) or streptozotocin (FVBN + STZ or Tg26 + STZ). After two weeks, biomarkers were collected and kidneys were harvested. FVBN + STZ and Tg26 + STZ displayed elevated serum glucose levels when compared to FVBN and Tg26 respectively. Tg26 + STZ displayed elevated (P < 0.05) blood urea nitrogen (BUN) levels (P < 0.05) and enhanced (P < 0.01) proteinuria when compared to Tg26. Tg26 + STZ displayed enhanced (P < 0.001) number of sclerotic glomeruli and microcysts vs. Tg26. Renal tissues of Tg26 displayed down regulation of vitamin D receptor (VDR) expression and enhanced Ang II production when compared to FVBN mice. Hyperglycemia exacerbated down regulation of VDR and production of Ang II in FVBN and Tg mice. Hyperglycemia increased kidney cell reactive oxygen species (ROS) production and oxidative DNA damage in both FVBN and Tg26 mice. In in vitro studies, HIV down regulated podocyte VDR expression and also enhanced renin angiotensin system activation. In addition, both glucose and HIV stimulated kidney cell ROS generation and DNA damage and compromised DNA repair; however, tempol (superoxide dismutase mimetic), losartan (Ang II blocker) and EB1089 (VDR agonist) provided protection against DNA damaging effects of glucose and HIV. These findings indicated that glucose activated the RAS and inflicted oxidative stress-mediated DNA damage via down regulation of kidney cell VDR expression in HIV milieu both in vivo and in vitro.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 27, Issue 3, March 2015, Pages 460-469
Journal: Cellular Signalling - Volume 27, Issue 3, March 2015, Pages 460-469
نویسندگان
Partab Rai, Tejinder Singh, Rivka Lederman, Amrita Chawla, Dileep Kumar, Kang Cheng, Gautam Valecha, Peter W. Mathieson, Moin A. Saleem, Ashwani Malhotra, Pravin C. Singhal,