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Titolo:
Domains of apolipoprotein E contributing to triglyceride and cholesterol homeostasis in vivo - Carboxyl-terminal region 203-299 promotes hepatic verylow density lipoprotein-triglyceride secretion
Autore:
Kypreos, KE; van Dijk, KW; van der Zee, A; Havekes, LM; Zannis, VI;
Indirizzi:
Boston Univ, Sch Med, Dept Med, Whitaker Cardiovasc Inst, Boston, MA 02118USA Boston Univ Boston MA USA 02118 aker Cardiovasc Inst, Boston, MA 02118USA Leiden Univ, Med Ctr, Dept Human & Clin Genet, NL-2333 AL Leiden, Netherlands Leiden Univ Leiden Netherlands NL-2333 AL NL-2333 AL Leiden, Netherlands TNO PG Prevent & Hlth, Gaubius Lab, NL-2333 CK Leiden, Netherlands TNO PG Prevent & Hlth Leiden Netherlands NL-2333 CK Leiden, Netherlands Univ Crete, Dept Biochem, Heraklion 71110, Crete, Greece Univ Crete Heraklion Crete Greece 71110 m, Heraklion 71110, Crete, Greece Univ Crete, Inst Mol Biol & Biotechnol, Heraklion 71110, Crete, Greece Univ Crete Heraklion Crete Greece 71110 l, Heraklion 71110, Crete, Greece
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 23, volume: 276, anno: 2001,
pagine: 19778 - 19786
SICI:
0021-9258(20010608)276:23<19778:DOAECT>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
E-DEFICIENT MICE; RECEPTOR-BINDING DOMAIN; TRANSGENIC MICE; III HYPERLIPOPROTEINEMIA; APO-E; ATHEROSCLEROSIS; VARIANT; PLASMA; DIET; HYPERTRIGLYCERIDEMIA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
61
Recensione:
Indirizzi per estratti:
Indirizzo: Zannis, VI Boston Univ, Sch Med, Dept Med, Whitaker Cardiovasc Inst, 715 Albany St,W509, Boston, MA 02118 USA Boston Univ 715 Albany St,W509 Boston MA USA 02118 MA 02118 USA
Citazione:
K.E. Kypreos et al., "Domains of apolipoprotein E contributing to triglyceride and cholesterol homeostasis in vivo - Carboxyl-terminal region 203-299 promotes hepatic verylow density lipoprotein-triglyceride secretion", J BIOL CHEM, 276(23), 2001, pp. 19778-19786

Abstract

Apolipoprotein (apo)E has been implicated in cholesterol. and triglyceridehomeostasis in humans. At physiological concentration apoE promotes efficient clearance of apoE-containing lipoprotein remnants. However, high apoE plasma levels correlate with high plasma triglyceride levels. We have used adenovirus-mediated gene transfer in apoE-deficient mice (E-/-) to define the domains of apoE required for cholesterol and triglyceride homeostasis in,vivo. A dose of 2 x 10(9) plaque-forming units of apoE4-expressing adenovirus reduced slightly the cholesterol levels of E-/- mice and resulted in severe hypertriglyceridemia, due to accumulation of cholesterol and triglyceride-rich very low density Lipoprotein particles in plasma, In contrast, thetruncated form apoE4-202 resulted in a 90% reduction in the plasma cholesterol levels but did not alter plasma triglyceride levels in the E-/- mice. ApoE secretion by cell cultures, as well as the steady-state hepatic mRNA levels in individual mice expressing apoE4 or apoE4-202, were similar. In contrast, very low density lipoprotein-triglyceride secretion in mice expressing apoE4, but not, apoE4-202, was increased 10-fold, as compared with miceinfected with a control adenovirus, The findings suggest that the amino-terminal 1-202 region of apoE4 contains the domains required for the in vivo clearance of Lipoprotein remnants. Furthermore, the carboxyl-terminal 203-299 residues of apoE promote hepatic very low density lipoprotein-triglyceride secretion and contribute to apoE-induced hypertriglyceridemia.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/01/20 alle ore 19:08:35