Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
OVEREXPRESSION OF HUMAN APOLIPOPROTEIN-A-I IN TRANSGENIC RATS AND THEHYPERLIPOPROTEINEMIA ASSOCIATED WITH EXPERIMENTAL NEPHROSIS
Autore:
BURKEY BF; FRANCE D; WANG HX; MA XW; BRAND B; ABUHANI C; DIFFENDERFER MR; MARSH JB; PATERNITI JR; FISHER EA;
Indirizzi:
SANDOZ PHARMACEUT CORP,SANDOZ RES INST,DEPT METAB DIS E HANOVER NJ 07936 MED COLL PENN,DEPT BIOCHEM PHILADELPHIA PA 19129
Titolo Testata:
Journal of lipid research
fascicolo: 7, volume: 36, anno: 1995,
pagine: 1463 - 1473
SICI:
0022-2275(1995)36:7<1463:OOHAIT>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
DIET-INDUCED HYPERCHOLESTEROLEMIA; MESSENGER-RNA LEVEL; GENE-EXPRESSION; APOA-I; HYPERLIPIDEMIA; LIVER; LIPOPROTEINS; SECRETION; DECREASE; INJURY;
Keywords:
HIGH DENSITY LIPOPROTEIN; KIDNEY DISEASE; PUROMYCIN AMINONUCLEOSIDE; HYPERLIPIDEMIA; PROTEINURIA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
36
Recensione:
Indirizzi per estratti:
Citazione:
B.F. Burkey et al., "OVEREXPRESSION OF HUMAN APOLIPOPROTEIN-A-I IN TRANSGENIC RATS AND THEHYPERLIPOPROTEINEMIA ASSOCIATED WITH EXPERIMENTAL NEPHROSIS", Journal of lipid research, 36(7), 1995, pp. 1463-1473

Abstract

Hyperlipoproteinemia contributes both to kidney disease progression and the development of atherosclerosis. Elevated high density lipoprotein cholesterol and apolipoprotein A-I (apoA-I) serum levels are independent factors protective against the atherosclerotic process. We examined the effects in a transgenic rat model of human apoA-I expression on the hyperlipoproteinemia and edema after puromycin aminonucleoside-induced nephrosis in three groups of animals: low line (TgR[hAI](low), human plasma apoA-I = 16.0 mg/dl); high line (TgR[hAI](high), 284 mg/dl); and non-transgenic litter mates (TgR[hAI](non)). Nephrosis increased total plasma apoA-I levels 2-fold in TgR[hAI](non) rats (75 vs. 162mg/dl) and 4-fold in the TgR[hAI](low) (97 vs. 458 mg/dl) and TgR[hAI](high) rats (356 vs. 1,346 mg/dl). In both transgenic lines, this increase was due mainly to elevations of serum human apoA-I. The hepatic steady-state levels of rat apoA-I mRNA increased 5- to 7-fold in all three groups, while human apoA-I mRNA levels increased 21- and 65-fold in the low and high expressing groups, respectively, indicating a different degree of responsiveness of the rat and human genes. While nephrotic TgR[hAI](non) and TgR[hAI](low) rats showed severe hyperlipoproteinemia and edema, much lower levels of edema and of serum triglycerides, phospholipids, and cholesterol were seen in the TgR[hAI](high) group. Urinary excretion of apoA-I, phospholipids, and cholesterol was significantly increased in the TgR[hAI](high) group, indicating this as one possible mechanism for the relatively lower serum levels of these lipids. We conclude that the human apoA-I gene is responsive to nephrosis and that human apoA-I-transgenic rats with this syndrome provide ananimal model for the study of human high density lipoprotein and apoA-I metabolism.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/07/20 alle ore 05:41:06