期刊
ARCHIVES OF MEDICAL RESEARCH
卷 43, 期 1, 页码 11-14出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.arcmed.2012.01.001
关键词
Low-density lipoprotein cholesterol; Lp-PLA(2); PCSK9
资金
- National Health and Research Council (Australia) [1010867]
Background and Aims. Lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) is a proatherogenic phospholipase A(2), which is predominantly complexed to low-density lipoprotein (LDL) particles. Proprotein convertase subtilisin-kexin type 9 (PCSK9) provides a key step in LDL metabolism by stimulating LDL receptor degradation. We determined relationships between plasma PCSK9 and Lp-PLA(2) mass. Methods. Lp-PLA(2) mass (turbidimetric immunoassay), PCSK9 (enzyme-linked immunosorbent assay) and (apo) lipoproteins were measured in 53 nondiabetic subjects (27 women) with body mass index <30 kg/m(2). Results. Lp-PLA(2) and PCSK9 levels were both correlated positively with LDL cholesterol and non-high-density lipoprotein (HDL) cholesterol (r = 0.330 to r = 0.382, p <= 0.02). Remarkably, Lp-PLA(2) was inversely related to PCSK9 (r = -0.388, p = 0.004). The Lp-PLA(2)/apolipoprotein B ratio, as a measure of the Lp-PLA(2) content in apolipoprotein B-containing lipoproteins, was also inversely correlated with PCSK9 (r = -0.575, p <0.001). The inverse relationships of Lp-PLA(2) (p = 0.023) and the Lp-PLA(2)/apolipoprotein B ratio (p = 0.001) with PCSK9 levels remained significant after controlling for age, gender, triglycerides and HDL cholesterol. Conclusions. Despite increasing effects on LDL cholesterol, higher PCSK9 levels are unlikely to confer impaired Lp-PLA(2) metabolism. We propose to evaluate the possible influence of PCSK9 inhibiting strategies on Lp-PLA(2) regulation and vice versa to determine effects of Lp-PLA(2) inhibitors on the PCSK9 pathway. (C) 2012 IMSS. Published by Elsevier Inc.
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