angiotensinogen and AIDS-Associated-Nephropathy
angiotensinogen has been researched along with AIDS-Associated-Nephropathy* in 2 studies
Other Studies
2 other study(ies) available for angiotensinogen and AIDS-Associated-Nephropathy
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Hyperglycemia enhances kidney cell injury in HIVAN through down-regulation of vitamin D receptors.
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. Topics: AIDS-Associated Nephropathy; Angiotensinogen; Animals; Cells, Cultured; Down-Regulation; gag Gene Products, Human Immunodeficiency Virus; Glucose; HEK293 Cells; HIV-1; Humans; Hyperglycemia; Kidney Glomerulus; Mice; Mice, Transgenic; Podocytes; pol Gene Products, Human Immunodeficiency Virus; Proteinuria; Reactive Oxygen Species; Receptors, Calcitriol; Streptozocin | 2015 |
Adverse host factors exacerbate occult HIV-associated nephropathy.
In the present study, we hypothesized that HIV-1-induced occult HIV-associated nephropathy (HIVAN) would become apparent in the presence of adverse host factors. To test our hypothesis, Vpr mice (which display doxycycline-dependent Vpr expression in podocytes) with two, three, and four copies of the angiotensinogen (Agt) gene (Vpr-Agt-2, Vpr-Agt-3, and Vpr-Agt-4) were administered doxycycline for 3 weeks (to develop clinically occult HIVAN) followed by doxycycline-free water during the next 3 weeks. Subsequently, renal biomarkers were measured, and kidneys were harvested for renal histology. Vpr-Agt-2 developed neither proteinuria nor elevated blood pressure, and displayed minimal glomerular and tubular lesions only, without any microcyst formation. Vpr-Agt-3 showed mild glomerular and tubular lesions and microcyst formation, whereas Vpr-Agt-4 showed moderate proteinuria, hypertension, glomerular sclerosis, tubular dilation, microcysts, and expression of epithelial mesenchymal transition markers. Vpr-Agt-4 not only displayed enhanced renal tissue expression of Agt, renin, and angiotensin-converting enzyme, but also had higher renal tissue concentrations of angiotensin II. Moreover, renal cells in Vpr-Agt-4 showed enhanced expression of transforming growth factor-β, connective tissue growth factor, and vascular endothelial growth factor. These findings indicate that adverse host factors, such as the activation of the renin-angiotensin system, promote the progression of occult HIVAN to apparent HIVAN. Topics: AIDS-Associated Nephropathy; Angiotensin II; Angiotensinogen; Animals; Biomarkers; Blood Pressure; Connective Tissue Growth Factor; Doxycycline; Epithelial-Mesenchymal Transition; Female; Gene Dosage; Genes, vpr; Host-Pathogen Interactions; Kidney; Male; Mice; Mice, Transgenic; Peptidyl-Dipeptidase A; Phenotype; Proteinuria; Renin; Renin-Angiotensin System; Transforming Growth Factor beta; Vascular Endothelial Growth Factor A | 2011 |