Lipoprotein-associated phospholipase A2

Phospholipase A2, group VII (platelet-activating factor acetylhydrolase, plasma)

Rendering based on PDB 3D59.
Identifiers
Symbols PLA2G7; LDL-PLA2; LP-PLA2; PAFAH
External IDs OMIM601690 MGI1351327 HomoloGene3725 GeneCards: PLA2G7 Gene
EC number 3.1.1.47
RNA expression pattern
More reference expression data
Orthologs
Species Human Mouse
Entrez 7941 27226
Ensembl ENSG00000146070 ENSMUSG00000023913
UniProt Q13093 Q3U1V7
RefSeq (mRNA) NM_001168357.1 NM_013737.5
RefSeq (protein) NP_001161829.1 NP_038765.2
Location (UCSC) Chr 6:
46.67 – 46.7 Mb
Chr 17:
43.71 – 43.75 Mb
PubMed search [1] [2]

Lipoprotein-associated phospholipase A2 (Lp-PLA2) also known as platelet-activating factor acetylhydrolase (PAF-AH) is a phospholipase A2 enzyme that in humans is encoded by the PLA2G7 gene.[1][2] Lp-PLA2 is a 45-kDa protein of 441 amino acids.[3]

Contents

Function

In the blood it travels mainly with low-density lipoprotein (LDL). Less than 20% is associated with high-density lipoprotein HDL. It is an enzyme produced by inflammatory cells and hydrolyzes oxidized phospholipids in LDL.

Lp-PLA2 is platelet-activating factor (PAF) acetylhydrolase (EC 3.1.1.47), a secreted enzyme that catalyzes the degradation of PAF to inactive products by hydrolysis of the acetyl group at the sn-2 position, producing the biologically inactive products LYSO-PAF and acetate.[4]

Clinical significance

Lp-PLA2 is involved in the development of atherosclerosis.[3] In human atherosclerotic lesions, 2 main sources of Lp-PLA2 can be identified, including that which is brought into the intima bound to LDL (from the circulation), and that which is synthesized de novo by plaque inflammatory cells (macrophages, T cells, mast cells)."

It is used as a marker for cardiac disease.[5]

A meta-analysis involving a total of 79,036 participants in 32 prospective studies found that Lp-PLA2 levels are positively correlated with increased risk of developing coronary heart disease and stroke.[6]

References

  1. ^ Tjoelker LW, Wilder C, Eberhardt C, Stafforini DM, Dietsch G, Schimpf B, Hooper S, Le Trong H, Cousens LS, Zimmerman GA (April 1995). "Anti-inflammatory properties of a platelet-activating factor acetylhydrolase". Nature 374 (6522): 549–53. doi:10.1038/374549a0. PMID 7700381. 
  2. ^ Tew DG, Southan C, Rice SQ, Lawrence MP, Li H, Boyd HF, Moores K, Gloger IS, Macphee CH (April 1996). "Purification, properties, sequencing, and cloning of a lipoprotein-associated, serine-dependent phospholipase involved in the oxidative modification of low-density lipoproteins". Arterioscler. Thromb. Vasc. Biol. 16 (4): 591–9. doi:10.1161/01.ATV.16.4.591. PMID 8624782. 
  3. ^ a b Zalewski A, Macphee C (May 2005). "Role of lipoprotein-associated phospholipase A2 in atherosclerosis: biology, epidemiology, and possible therapeutic target". Arterioscler. Thromb. Vasc. Biol. 25 (5): 923–31. doi:10.1161/01.ATV.0000160551.21962.a7. PMID 15731492. 
  4. ^ "Entrez Gene: PLA2G7 phospholipase A2, group VII (platelet-activating factor acetylhydrolase, plasma)". http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=7941. 
  5. ^ Mohler ER, Ballantyne CM, Davidson MH, Hanefeld M, Ruilope LM, Johnson JL, Zalewski A (April 2008). "The effect of darapladib on plasma lipoprotein-associated phospholipase A2 activity and cardiovascular biomarkers in patients with stable coronary heart disease or coronary heart disease risk equivalent: the results of a multicenter, randomized, double-blind, placebo-controlled study". J. Am. Coll. Cardiol. 51 (17): 1632–41. doi:10.1016/j.jacc.2007.11.079. PMID 18436114. 
  6. ^ The Lp-PLA2 Studies Collaboration (2010). "Lipoprotein-associated phospholipase A2 and risk of coronary disease, stroke, and mortality: collaborative analysis of 32 prospective studies". The Lancet 375 (9725): 1536–1544. doi:10.1016/S0140-6736(10)60319-4. Lay summary – BBC News. 

See also

Further reading