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Titolo:
Retrovirus-mediated expression of apolipoprotein A-I in the macrophage protects against atherosclerosis in vivo
Autore:
Ishiguro, H; Yoshida, H; Major, AS; Zhu, TL; Babaev, VR; Linton, MF; Fazio, S;
Indirizzi:
Vanderbilt Univ, Med Ctr, Div Cardiovasc Med, Dept Med, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 Dept Med, Nashville, TN 37232 USA Vanderbilt Univ, Med Ctr, Dept Pediat, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 pt Pediat, Nashville, TN 37232 USA Vanderbilt Univ, Med Ctr, Dept Pharmacol, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 Pharmacol, Nashville, TN 37232 USA Vanderbilt Univ, Med Ctr, Dept Pathol, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 pt Pathol, Nashville, TN 37232 USA
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 39, volume: 276, anno: 2001,
pagine: 36742 - 36748
SICI:
0021-9258(20010928)276:39<36742:REOAAI>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
HIGH-DENSITY-LIPOPROTEIN; BINDING CASSETTE TRANSPORTER-1; APOE-DEFICIENT MICE; TANGIER-DISEASE; GENE-EXPRESSION; TRANSGENIC MICE; BONE-MARROW; CHOLESTEROL; PLASMA; MOUSE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
32
Recensione:
Indirizzi per estratti:
Indirizzo: Fazio, S Vanderbilt Univ, Med Ctr, Div Cardiovasc Med, Dept Med, 315 Med Res Bldg 2, Nashville, TN 37232 USA Vanderbilt Univ 315 Med Res Bldg 2 Nashville TN USA 37232 232 USA
Citazione:
H. Ishiguro et al., "Retrovirus-mediated expression of apolipoprotein A-I in the macrophage protects against atherosclerosis in vivo", J BIOL CHEM, 276(39), 2001, pp. 36742-36748

Abstract

We have previously reported that the lack of apolipoprotein (apo) E expression by macrophages promotes foam cell formation in vivo. Because transgenic mice overexpressing human apoA-I from the liver (h-apoA-I TgN) are protected from the atherogenesis induced by apoE deficiency, we hypothesized thatthe presence of apoA-I in the vessel wall could reduce the negative effectof apoE deficiency on lesion growth. To address this issue, we used both retroviral transduction and transgenic approaches to produce in vivo systemswhere apoA-I is expressed from macrophages. In the retroviral transductionstudy, apoA-I-deficient (apoA-I-/-) mice reconstituted with apoE-deficient(apoE(-/-)) bone marrow cells that were infected with a retroviral vector expressing human apoA-I (MFG-HAI) had 95% lower atherosclerotic lesion areathan that of recipients of apoE(-/-) bone marrow cells infected with the parental virus (MFG). To determine whether the protective effect of locally produced apoA-I was due to the lack of systemic apoA-I, we conducted a different experiment using h-apoA-I TgN mice as recipients of apoE(-/-) bone marrow with or without human apoA-I (driven by a macrophage-specific transgene defined as m phi -AI). Aortic lesion area in apoE(-/-)/m phi -Al --> h-apoA-I TgN mice was decreased by 85% compared with apoE(-/-) --> h-apoA-I TgNmice. These data demonstrate that expression of apoA-I from macrophages protects against atherogenesis without affecting plasma apoA-I and high density lipoprotein cholesterol levels.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 06:53:00