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Titolo:
CELLULAR UPTAKE OF LIPOPROTEIN[A] BY MOUSE EMBRYONIC FIBROBLASTS VIA THE LDL RECEPTOR AND THE LDL RECEPTOR-RELATED PROTEIN
Autore:
REBLIN T; NIEMEIER A; MEYER N; WILLNOW TE; KRONENBERG F; DIEPLINGER H; GRETEN H; BEISIEGEL U;
Indirizzi:
UNIV HAMBURG,HOSP EPPENDORF,MED CLIN,MARTINISTR 52 D-20246 HAMBURG GERMANY MAX DELBRUCK CTR MOL MED BERLIN GERMANY INNSBRUCK UNIV,INST MED BIOL & HUMAN GENET A-6020 INNSBRUCK AUSTRIA
Titolo Testata:
Journal of lipid research
fascicolo: 10, volume: 38, anno: 1997,
pagine: 2103 - 2110
SICI:
0022-2275(1997)38:10<2103:CUOLBM>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
LOW-DENSITY-LIPOPROTEIN; HUMAN MONOCYTE-MACROPHAGES; COA REDUCTASE INHIBITOR; FAMILIAL HYPERCHOLESTEROLEMIA; LP(A) LIPOPROTEIN; APOLIPOPROTEIN(A) PHENOTYPE; CULTURED FIBROBLASTS; BABOON HEPATOCYTES; MONKEY MODEL; PLASMA;
Keywords:
APOLIPOPROTEIN[A]; LOW DENSITY LIPOPROTEIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
56
Recensione:
Indirizzi per estratti:
Citazione:
T. Reblin et al., "CELLULAR UPTAKE OF LIPOPROTEIN[A] BY MOUSE EMBRYONIC FIBROBLASTS VIA THE LDL RECEPTOR AND THE LDL RECEPTOR-RELATED PROTEIN", Journal of lipid research, 38(10), 1997, pp. 2103-2110

Abstract

The sites and precise mechanisms of the catabolism of the atherogeniclipoprotein[a] (Lp[al) are unknown. It has been proposed that the lowdensity lipoprotein receptor (LDL-R) and the low density lipoprotein receptor-related protein (LRP) are involved in the catabolism of Lp [a]. To address the question whether and to what extent the LDL-R and/orLRP are involved in the catabolism of Lp[a], we studied die cellular uptake of Lp [a] via those two receptors using mouse embryonic fibroblast (MEF) cell lines lacking either the LDL-R, the LRP, or both receptors due to disruption of the respective mouse genes. I-125-labeled LDLand I-125-labeled Lp[a] uptake by wild-type fibroblasts (MEF1) was compared with that by fibroblasts homozygous for the disrupted LRP allele (MEF2), fibroblasts with two defective alleles for the LDLR (MEF2), and fibroblasts homozygous for defects both in the LDL-R and LRP gene (MEF4). Compared with MEF1, I-125-labeled LDL uptake by MEF2 was 77%, by MEFS 30%, and by MEF4 24% of that by MEF1. However, no significant differences in the specific I-125-labeled Lp[al uptake by the four mouse embryonic cell lines was observed. In comparison with MEF1, the I-125-labeled Lp[a] uptake by MEF2 was 98%, by MEFS 111%, and 73% by MEF4. Approximately 50% of the total cellular uptake of I-125-labeled Lp[a] was nonspecific. In conclusion, our results suggest that Lp[a] is a poor ligand for the LDL receptor and die LRP. The data of the displacement studies, however, indicated that the nonspecific uptake of Lp [a]constitutes a major route for the cellular Lp [a] catabolism in this study.

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Documento generato il 17/02/20 alle ore 08:18:18