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Titolo:
AGEs induce oxidative stress and activate protein kinase C-beta(II) in neonatal mesangial cells
Autore:
Scivittaro, V; Ganz, MB; Weiss, MF;
Indirizzi:
Univ Hosp Cleveland, Dept Med, Div Nephrol, Cleveland, OH 44124 USA Univ Hosp Cleveland Cleveland OH USA 44124 phrol, Cleveland, OH 44124 USA Case Western Reserve Univ, Dept Med, Div Nephrol, Cleveland, OH 44106 USA Case Western Reserve Univ Cleveland OH USA 44106 Cleveland, OH 44106 USA Vet Adm Med Ctr, Cleveland, OH 44106 USA Vet Adm Med Ctr Cleveland OH USA44106 m Med Ctr, Cleveland, OH 44106 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
fascicolo: 4, volume: 278, anno: 2000,
pagine: F676 - F683
SICI:
0363-6127(200004)278:4<F676:AIOSAA>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLYCATION END-PRODUCTS; EXTRACELLULAR-MATRIX SYNTHESIS; GROWTH-FACTOR; FLUORESCENT-PROBES; MAILLARD REACTION; OXIDANT STRESS; PKC ISOFORMS; RECEPTOR; EXPRESSION; DISEASE;
Keywords:
advanced glycation end products; protein kinase C isoforms; intracellular oxidative stress; mesangial cells; neonatal rat mesangial cells;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Weiss, MF Univ Hosp Cleveland, Dept Med, Div Nephrol, 11100 Euclid Ave, Cleveland, OH 44124 USA Univ Hosp Cleveland 11100 Euclid Ave Cleveland OH USA44124 USA
Citazione:
V. Scivittaro et al., "AGEs induce oxidative stress and activate protein kinase C-beta(II) in neonatal mesangial cells", AM J P-REN, 278(4), 2000, pp. F676-F683

Abstract

Increased activation of specific protein kinase C (PKC) isoforms and increased nonenzy matic glycation of intracellular and extracellular proteins [the accumulation of advanced glycation end products (AGEs)] are major mechanistic pathways implicated in the pathogenesis of diabetic complications. Blocking PKC-beta(II) has been shown to decrease albuminuria in animal modelsof diabetes. To demonstrate a direct relationship between AGEs and the induction and translocation of PKC-beta(II), studies were carried out in rat neonatal mesangial cells, known to express PKC-beta(II) in association with rapid proliferation in post-natal development. Oxidative stress was studiedby using the fluorescent probe dichlorfluorescein diacetate. Translocationof PKC-beta(II) was demonstrated by using immunofluorescence and Western blotting of fractionated mesangial cells. Induction of intracellular oxidative stress, increase in intracellular calcium, and cytosol to membrane PKC-beta(II) translocation (with no change in PKC-alpha) were demonstrated afterexposure to AGE-rich proteins. These data support the hypothesis that AGEscause mesangial oxidative stress and alterations in PKC-beta(II), changes that may ultimately contribute to phenotypic abnormalities associated with diabetic nephropathy.

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Documento generato il 22/10/20 alle ore 12:42:20