| First Author | Boyanovsky B | Year | 2009 |
| Journal | Arterioscler Thromb Vasc Biol | Volume | 29 |
| Issue | 4 | Pages | 532-8 |
| PubMed ID | 19164803 | Mgi Jnum | J:159779 |
| Mgi Id | MGI:4452435 | Doi | 10.1161/ATVBAHA.108.183038 |
| Citation | Boyanovsky B, et al. (2009) The capacity of group V sPLA2 to increase atherogenicity of ApoE-/- and LDLR-/- mouse LDL in vitro predicts its atherogenic role in vivo. Arterioscler Thromb Vasc Biol 29(4):532-8 |
| abstractText | OBJECTIVE: In vitro data indicate that human LDL modified by Group V secretory phospholipase A(2) (GV sPLA(2)) is proatherogenic. Consistent with this, gain and loss of function studies demonstrated that GV sPLA(2) promotes atherosclerosis in LDLR(-/-) mice. The current study investigates whether GV sPLA(2) promotes atherosclerotic processes in apoE(-/-) mice. METHODS AND RESULTS: LDL (d=1.019 to 1.063) from apoE(-/-) and LDLR(-/-) mice fed chow or Western diet were hydrolyzed by GV sPLA(2). Phosphatidylcholine on LDL from LDLR(-/-) mice fed either a chow or Western diet was hydrolyzed to a greater extent (61.1+/-0.4% and 45.3+/-4.6%) than the corresponding fractions from apoE(-/-) mice (41.7+/-3.6% and 39.4+/-1.2%). ApoE(-/-) LDL induced macrophage foam cell formation in vitro without modification by GV sPLA(2), whereas hydrolysis of LDLR(-/-) LDL was a prerequisite for foam cell formation. In contrast to findings in LDLR(-/-) mice, GV sPLA(2) deficiency did not significantly reduce atherosclerosis in apoE(-/-) mice, although collagen content was significantly reduced in lesions of apoE(-/-) mice lacking GV sPLA(2). CONCLUSIONS: The ability of GV sPLA(2) to promote atherosclerotic lipid deposition in apoE(-/-) and LDLR(-/-) mice may be related to its ability to increase the atherogenic potential of LDL from these mice as assessed in vitro. |
