Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Apoptosis induced by oxidized low density lipoprotein in human monocyte-derived macrophages involves CD36 and activation of caspase-3
Autore:
Wintergerst, ES; Jelk, J; Rahner, C; Asmis, R;
Indirizzi:
Univ Basel, Inst Biochem, CH-4003 Basel, Switzerland Univ Basel Basel Switzerland CH-4003 Biochem, CH-4003 Basel, Switzerland Univ Basel, Inst Anat, CH-4003 Basel, Switzerland Univ Basel Basel Switzerland CH-4003 st Anat, CH-4003 Basel, Switzerland
Titolo Testata:
EUROPEAN JOURNAL OF BIOCHEMISTRY
fascicolo: 19, volume: 267, anno: 2000,
pagine: 6050 - 6058
SICI:
0014-2956(200010)267:19<6050:AIBOLD>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN ATHEROSCLEROTIC PLAQUES; FOAM CELL-FORMATION; SCAVENGER RECEPTOR; ENDOTHELIAL-CELLS; POTENTIAL ROLE; SMOOTH-MUSCLE; SR-BI; EXPRESSION; IDENTIFICATION; LDL;
Keywords:
apoptosis; CD36; human macrophages; oxidized LDL; caspase-3;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
52
Recensione:
Indirizzi per estratti:
Indirizzo: Asmis, R Univ Kentucky, Div Cardiovasc Med, Kentucky Clin 543, 740 S Limestone, Lexington, KY 40536 USA Univ Kentucky 740 S Limestone Lexington KY USA 40536 KY 40536 USA
Citazione:
E.S. Wintergerst et al., "Apoptosis induced by oxidized low density lipoprotein in human monocyte-derived macrophages involves CD36 and activation of caspase-3", EUR J BIOCH, 267(19), 2000, pp. 6050-6058

Abstract

Macrophage death may play a crucial role in the progression of atherosclerotic lesions. Here we present evidence that CD36 is involved in oxidized LDL (OxLDL)-induced apoptosis in human monocyte-derived macrophages. Anti-CD36 mAb SMO and OKM-5 reduced the number of apoptotic cells in OxLDL-treated macrophages by more than 94%, but they did not block ceramide-triggered apoptosis. Thrombospondin inhibited the induction of apoptosis by OxLDL in a dose-dependent manner with an IC50 of 10-30 mu M. OxLDL did not induce apoptosis in CD36-negative macrophages, demonstrating the essential role of thisscavenger receptor in OxLDL-triggered programmed cell death. Neither anti-CD36 Ig nor thrombospondin triggered programmed cell death suggesting that binding to CD36 alone is not sufficient to initiate apoptosis. However, inhibitors of OxLDL-induced apoptosis did not block the uptake of H-3-labeled OxLDL. In contrast, acetylated LDL and polyinosinic acid, ligands of scavenger receptor A (SRA), inhibited uptake of H-3-labeled OxLDL by 65 and 49%, respectively, but did not block OxLDL-induced apoptosis, indicating that SRA is not involved in this process. OxLDL also stimulated caspase-3 activityin human macrophages. Activation of caspase-3 was blocked by anti-CD36 Ig and the caspase-3 inhibitor Z-DEVD-FMK. These results suggest that binding of OxLDL to CD36 initiates a yet unknown OxLDL-specific signaling event, which leads to the rapid activation of caspase-3 resulting in apoptosis of human macrophages. Our data demonstrate a novel role for CD36 in macrophage biology with likely consequences for the development of atherosclerotic lesions.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/09/20 alle ore 23:16:27