| First Author | Wooton-Kee CR | Year | 2004 |
| Journal | Arterioscler Thromb Vasc Biol | Volume | 24 |
| Issue | 4 | Pages | 762-7 |
| PubMed ID | 14962950 | Mgi Jnum | J:285014 |
| Mgi Id | MGI:6393145 | Doi | 10.1161/01.ATV.0000122363.02961.c1 |
| Citation | Wooton-Kee CR, et al. (2004) Group V sPLA2 hydrolysis of low-density lipoprotein results in spontaneous particle aggregation and promotes macrophage foam cell formation. Arterioscler Thromb Vasc Biol 24(4):762-7 |
| abstractText | OBJECTIVE: Secretory phospholipase A2 (sPLA2) enzymes hydrolyze the sn-2 fatty acyl ester bond of phospholipids to produce a free fatty acid and a lysophospholid. Group V sPLA2 is expressed in cultured macrophage cells and has high affinity for phosphatidyl choline-containing substrates. The present study assesses the presence of group V sPLA2 in human and mouse atherosclerotic lesions and its activity toward low-density lipoprotein (LDL) particles. METHODS AND RESULTS: Group V sPLA2 was detected in human and mouse atherosclerotic lesions by immunohistochemical staining. Electron microscopic analysis showed that mouse group V sPLA2-modified LDL is significantly smaller (mean diameter+/-SEM=25.3+/-0.25 nm) than native LDL (mean diameter+/-SEM=27.7+/-0.29 nm). Hydrolysis by group V sPLA2 induced spontaneous particle aggregation; the extent of aggregation was directly proportional to the degree of LDL hydrolysis. Group V sPLA2 modification of LDL led to enhanced lipid accumulation in cultured mouse peritoneal macrophage cells. CONCLUSIONS: Group V sPLA2 may play an important role in promoting atherosclerotic lesion development by modifying LDL particles in the arterial wall, thereby enhancing particle aggregation, retention, and macrophage uptake. |
