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Titolo:
Accelerated diabetic glomerulopathy in galectin-3/AGE receptor 3 knockout mice
Autore:
Pugliese, G; Pricci, F; Iacobini, C; Leto, G; Amadio, L; Barsotti, P; Frigeri, L; Hsu, DK; Vlassara, H; Liu, FT; Di Mario, U;
Indirizzi:
Univ Roma La Sapienza, Dept Clin Sci, I-00161 Rome, Italy Univ Roma La Sapienza Rome Italy I-00161 t Clin Sci, I-00161 Rome, Italy Univ Roma La Sapienza, Dept Expt Med & Pathol, I-00161 Rome, Italy Univ Roma La Sapienza Rome Italy I-00161 d & Pathol, I-00161 Rome, Italy Ist Super Sanita, Lab Metab & Biochem Pathol, I-00161 Rome, Italy Ist Super Sanita Rome Italy I-00161 Biochem Pathol, I-00161 Rome, Italy Scripps Clin & Res Inst, Dept Mol & Expt Med, La Jolla, CA 92037 USA Scripps Clin & Res Inst La Jolla CA USA 92037 Med, La Jolla, CA 92037 USA La Jolla Inst Allergy & Immunol, San Diego, CA 92121 USA La Jolla Inst Allergy & Immunol San Diego CA USA 92121 iego, CA 92121 USA CUNY Mt Sinai Sch Med, New York, NY 10029 USA CUNY Mt Sinai Sch Med New York NY USA 10029 h Med, New York, NY 10029 USA
Titolo Testata:
FASEB JOURNAL
fascicolo: 13, volume: 15, anno: 2001,
pagine: 2471 - 2479
SICI:
0892-6638(200111)15:13<2471:ADGIGR>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLYCATION END-PRODUCTS; GENE-EXPRESSION; BINDING-PROTEIN; COMPETITIVE PCR; GROWTH-FACTOR; MATRIX; AGE; ACTIVATION; CELLS; IDENTIFICATION;
Keywords:
diabetic nephropathy; advanced glycation end products; advanced glycation end product receptors extracellular matrix;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
35
Recensione:
Indirizzi per estratti:
Indirizzo: Pugliese, G Dipartimento Sci Clin Endocrinol, Viale Policlin 155, I-00161 Rome, Italy Dipartimento Sci Clin Endocrinol Viale Policlin 155 Rome ItalyI-00161
Citazione:
G. Pugliese et al., "Accelerated diabetic glomerulopathy in galectin-3/AGE receptor 3 knockout mice", FASEB J, 15(13), 2001, pp. 2471-2479

Abstract

Several molecules were shown to bind advanced glycation end products (AGEs) in vitro, but it is not known whether they all serve as AGE receptors andwhich functional role they play in vivo. We investigated the role of galectin-3, a multifunctional lectin with (anti) adhesive and growth-regulating properties, as an AGE receptor and its contribution to the development of diabetic glomerular disease, using a knockout mouse model. Galectin-3 knockout mice obtained by gene ablation and the corresponding wild-type mice wererendered diabetic with streptozotocin and killed 4 months later, together with age-matched nondiabetic controls. Despite a comparable degree of metabolic derangement, galectin-3-deficient mice developed accelerated glomerulopathy vs. the wild-type animals, as evidenced by the more pronounced increase in proteinuria, extracellular matrix gene expression, and mesangial expansion. This was associated with a more marked renal/glomerular AGE accumulation, indicating it was attributable to the lack of galectin-3 AGE receptorfunction. The galectin-3-deficient genotype was associated with reduced expression of receptors implicated in AGE removal (macrophage scavenger receptor A and AGE-R1) and increased expression of those mediating cell activation (RAGE and AGE-R2). These results show that the galectin-3-regulated AGE receptor pathway is operating in vivo and protects toward AGE-induced tissue injury in contrast to that through RAGE.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 00:42:12