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Titolo:
Basic fibroblast growth factor in HIV-associated hemolytic uremic syndrome
Autore:
Ray, PE; Liu, XH; Xu, L; Rakusan, T;
Indirizzi:
George Washington Univ, Childrens Natl Med Ctr, Div Nephrol, Washington, DC USA George Washington Univ Washington DC USA Div Nephrol, Washington, DC USA
Titolo Testata:
PEDIATRIC NEPHROLOGY
fascicolo: 7, volume: 13, anno: 1999,
pagine: 586 - 593
SICI:
0931-041X(199909)13:7<586:BFGFIH>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
PLASMINOGEN-ACTIVATOR PRODUCTION; ENDOTHELIAL-CELLS; THROMBOTIC MICROANGIOPATHY; EXTRACELLULAR-MATRIX; EPITHELIAL-CELLS; HEPARAN-SULFATE; NEPHROPATHY; EXPRESSION; APOPTOSIS; INFECTION;
Keywords:
human immunodeficiency virus nephropathy basic fibroblast growth factor; heparan sulfate proteoglycans; receptors; pediatric acquired immunodeficiency syndrome;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
44
Recensione:
Indirizzi per estratti:
Indirizzo: Ray, PE Childrens Natl Med Ctr, Childrens Res Inst, Ctr 4, Room R-211,111 MichiganAve NW, Washington, DC 20010 USA Childrens Natl Med Ctr Room R-211,111 Michigan Ave NW Washington DC USA 20010
Citazione:
P.E. Ray et al., "Basic fibroblast growth factor in HIV-associated hemolytic uremic syndrome", PED NEPHROL, 13(7), 1999, pp. 586-593

Abstract

Endothelial injury is the primary pathogenic event leading to the renal thrombotic microangiopathic lesions typical of the hemolytic uremic syndrome (HUS). Basic fibroblast growth factor (bFGF) is an angiogenic growth factorreleased by injured endothelial cells. In a previous study we have found asignificant accumulation of bFGF in human immunodeficiency virus (HIV)-transgenic mice with renal disease. Here we investigated whether bFGF was accumulated in the circulation and kidneys of two children with HIV-associated HUS (HIV-HUS), and studied the mechanisms involved in this process. The plasma levels of bFGF in children with HIV-HUS (124+/-20 pg/ml) were increasedcompared with five children with HIV nephropathy (49+/-6 pg/ml) and twentyHIV-infected children without renal disease (26+/-4 pg/ml, P<0.001). Immunohistochemistry and receptor binding studies showed that bFGF was accumulated bound to heparan sulfate proteoglycans in renal glomeruli and interstitium surrounding renal tubules in MV-HUS kidneys. Basic FGF stimulated the proliferation of mesangial and urinary renal tubular epithelial cells isolated from both patients. These findings support the hypothesis that bFGF and its low-affinity binding sites may play a relevant role in modulating the process of glomerular and renal tubular regeneration during the acute stages of HIV-HUS. A follow-up study in a larger sample population is required to confirm these results.

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Documento generato il 29/11/20 alle ore 00:57:28