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Identification of Nucleolar Factors During HIV-1 Replication Through Rev Immunoprecipitation and Mass Spectrometry
Published on: June 26, 2019
Basic fibroblast growth factor in HIV-associated hemolytic uremic syndrome
1Center IV, Room R-211, Children's Research Institute, Children's National Medical Center, 111 Michigan Avenue N.W., Washington, DC 20010, USA, Pray@cnmc.org
Pediatric Nephrology (Berlin, Germany)
|August 25, 1999
Summary
Basic fibroblast growth factor (bFGF) accumulates in children with HIV-associated hemolytic uremic syndrome (HUS), potentially driving kidney regeneration. Further studies are needed to confirm bFGF
Area of Science:
- Nephrology
- Virology
- Cell Biology
Background:
- Endothelial injury initiates renal thrombotic microangiopathy in hemolytic uremic syndrome (HUS).
- Basic fibroblast growth factor (bFGF), an angiogenic factor, is released by injured endothelial cells.
- Previous research indicated bFGF accumulation in HIV-transgenic mice with renal disease.
Observation:
- This study investigated bFGF levels and mechanisms in children with HIV-associated HUS (HIV-HUS).
- Elevated plasma bFGF levels were observed in children with HIV-HUS compared to controls.
- Immunohistochemistry revealed bFGF bound to heparan sulfate proteoglycans in renal glomeruli and tubules of HIV-HUS kidneys.
Findings:
- Plasma bFGF levels were significantly higher in children with HIV-HUS (124 pg/ml) than in HIV nephropathy (49 pg/ml) or HIV-infected children without renal disease (26 pg/ml).
- bFGF accumulation was localized to renal glomeruli and interstitial areas surrounding tubules in HIV-HUS kidneys.
- Isolated mesangial and renal tubular epithelial cells from patients exhibited proliferation stimulated by bFGF.
Implications:
- bFGF may play a role in glomerular and tubular regeneration during acute stages of HIV-HUS.
- The findings suggest bFGF and its binding sites are relevant to HIV-HUS pathogenesis.
- Larger studies are required to validate these findings and their clinical significance.
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