Loss of lysophospholipase 3 increases atherosclerosis in apolipoprotein E-deficient mice.
Biochem Biophys Res Commun
; 330(1): 104-10, 2005 Apr 29.
Article
en En
| MEDLINE
| ID: mdl-15781238
ABSTRACT
Human LCAT-like lysophospholipase (LLPL), or lysophospholipase 3, was first identified in vitro, in foam cells derived from THP-1 cells. We demonstrated that LLPL was present in foam cells in the severe atherosclerotic lesions that develop in apolipoprotein E-null (apoE(-/-)) mice. This indicated that LLPL might affect lipid metabolisms in foam cells and, therefore, atherogenesis. Accordingly, we created LLPL-knockout mice by gene targeting and crossed them with apoE(-/-) mice. We showed that the absence of LLPL increased lesion formation markedly in apoE(-/-) mice but had little effect on the plasma-lipid profile. In addition, LLPL-deficient peritoneal macrophages were more sensitive to apoptosis induced by exposure to oxidized low-density lipoprotein. LLPL might provide a link between apoptosis in macrophages and atherogenesis. Our data demonstrate that LLPL activity is anti-atherogenic and indicate that the regulation of this enzyme might be a novel drug target for the treatment of atherosclerosis.
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Banco de datos:
MEDLINE
Asunto principal:
Apolipoproteínas E
/
Arteriosclerosis
/
Lisofosfolipasa
Límite:
Animals
Idioma:
En
Año:
2005
Tipo del documento:
Article