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Expression of HIV transgene aggravates kidney injury in diabetic mice.

Abstract
With the widespread use of combination antiretroviral agents, the incidence of HIV-associated nephropathy has decreased. Currently, HIV-infected patients live much longer and often suffer from comorbidities such as diabetes mellitus. Recent epidemiological studies suggest that concurrent HIV infection and diabetes mellitus may have a synergistic effect on the incidence of chronic kidney disease. To address this, we determined whether HIV-1 transgene expression accelerates diabetic kidney injury using a diabetic HIV-1 transgenic (Tg26) murine model. Diabetes was initially induced with low-dose streptozotocin in both Tg26 and wild-type mice on a C57BL/6 background, which is resistant to classic HIV-associated nephropathy. Although diabetic nephropathy is minimally observed on the C57BL/6 background, diabetic Tg26 mice exhibited a significant increase in glomerular injury compared with nondiabetic Tg26 mice and diabetic wild-type mice. Validation of microarray gene expression analysis from isolated glomeruli showed a significant upregulation of proinflammatory pathways in diabetic Tg26 mice. Thus, our study found that expression of HIV-1 genes aggravates diabetic kidney disease.
AuthorsSandeep K Mallipattu, Ruijie Liu, Yifei Zhong, Ed Y Chen, Vivette D'Agati, Lewis Kaufman, Avi Ma'ayan, Paul E Klotman, Peter Y Chuang, John C He
JournalKidney international (Kidney Int) Vol. 83 Issue 4 Pg. 626-34 (Apr 2013) ISSN: 1523-1755 [Electronic] United States
PMID23325078 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
Chemical References
  • Biomarkers
  • Collagen Type IV
  • Fusion Proteins, gag-pol
  • Inflammation Mediators
  • Smad3 Protein
  • Smad3 protein, mouse
  • Creatinine
Topics
  • Albuminuria (etiology, genetics, virology)
  • Animals
  • Biomarkers (urine)
  • Collagen Type IV (metabolism)
  • Creatinine (urine)
  • Diabetes Mellitus, Experimental (blood, complications, immunology)
  • Diabetic Nephropathies (etiology, genetics, immunology, pathology, urine, virology)
  • Disease Progression
  • Fibrosis
  • Fusion Proteins, gag-pol (genetics)
  • Gene Expression Profiling (methods)
  • HIV Infections (blood, complications, genetics, immunology, virology)
  • HIV-1 (genetics, immunology)
  • Inflammation Mediators (blood)
  • Kidney (immunology, metabolism, pathology, virology)
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Oligonucleotide Array Sequence Analysis
  • Phosphorylation
  • Real-Time Polymerase Chain Reaction
  • Reproducibility of Results
  • Smad3 Protein (metabolism)
  • Time Factors

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