| First Author | Taniyama Y | Year | 2005 |
| Journal | Biochem Biophys Res Commun | Volume | 330 |
| Issue | 1 | Pages | 104-10 |
| PubMed ID | 15781238 | Mgi Jnum | J:97471 |
| Mgi Id | MGI:3575488 | Doi | 10.1016/j.bbrc.2005.02.126 |
| Citation | Taniyama Y, et al. (2005) Loss of lysophospholipase 3 increases atherosclerosis in apolipoprotein E-deficient mice. Biochem Biophys Res Commun 330(1):104-10 |
| abstractText | 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. |
