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Persistently elevated serum concentrations of Lp-PLA2 were associated with an unfavorable outcome in patients with sepsis.
Resveratrol downregulates Lp-PLA2 expression by inhibiting oxidative stress via SIRT1 (show SIRT1 Proteins) pathway in the THP-1-derived macrophages.
Elevated Lp-PLA2 mass was associated with all cause-death independently of other risk factors within one year after acute ischemic stroke.
PLA2G7 and PON1 (show PON1 Proteins) are overexpressed in prostatic neoplasm patients and can be detected early in blood.
A PLA2G7 gene polymorphism determines the plasma levels of lipoprotein-associated phospholipase A2 activity and mass and manifests as a risk factor for atherosclerosis.
Conclusion RBP4 (show POLR2D Proteins) may be used as a predictive factor of diabetic nephropathy patients complicated with silent cerebral infarction (SCI) and is positively correlated with cognitive dysfunction. RBP4 (show POLR2D Proteins)/Lp-PLA2/Netrin-1 (show NTN1 Proteins) pathway activation may be one of the occurrence mechanisms in diabetic nephropathy complicated with SCI.
Greater Lp-PLA2 activity or mass was associated with an increased risk of CHD (show CHDH Proteins) and IS
Lp-PLA2 G994T gene polymorphism may be an independent risk factor of ischemic stroke in Chinese population.
Lifelong lower Lp-PLA2 activity was not associated with major risks of vascular or non-vascular diseases in Chinese adults.
phospholipase A2 (show YWHAZ Proteins) Group 7 (PLA2G7), to be important in regulating tumor cell migration and a novel tumor-promoting factor in nasopharyngeal carcinoma.
The results demonstrated that Lp-PLA2 is associated with triglycerides which may be helpful for understanding the relationship of this protein with cardiovascular disease.
Effect of splenectomy and autologous spleen transplantation on the serum PAF-AH activity and acute-phase response in a porcine model are reported.
observations support a proatherogenic role for Lp-PLA2
Variable gene expression (eg, matrix metalloproteinase-9 (show MMP9 Proteins), CCL2 (show CCL2 Proteins) and Lp-PLA(2) mRNAs), both in regard to the arterial bed and duration of disease, was associated with variable plaque development and progression.
The significant correlation between PLA2G7 RNA expression in plaque macrophages and plasma PAFAH activity suggests that the latter is a consequence, rather than a cause of macrophage accumulation.
Resveratrol downregulates Lp-PLA2 expression by inhibiting oxidative stress via SIRT1 (show SIRT1 Proteins) pathway in a mouse model of chronic inflammation.
Lp-PLA2 augments the inflammatory response after MI and antagonizes healing by disrupting the balance between inflammation and repair.
Plg (show PLG Proteins) from mouse plasma contains oxPtdPC adducts that are not affected by the action of Lp-PLA(2), suggesting that linkage to Plg (show PLG Proteins) protects oxPtdPCs from metabolism during their transport in the plasma.
SAA (show SAA1 Proteins) up-regulates Lp-PLA2 production significantly via a FPRL1 (show FPR2 Proteins)/MAPKs./PPAR-gamma (show PPARG Proteins) signaling pathway.
Deletion of Pla2g7 decreases small intestinal polyp and colon tumor incidence in ApcMin/+ mice.
Macrophage VLDL receptor (show VLDLR Proteins) promotes PAFAH (show PAFAH1B1 Proteins) secretion in mother's milk and suppresses systemic inflammation in nursing neonates.
Pla2g7 and Tnfrsf21 (show TNFRSF21 Proteins) have been identified as genetic susceptibility to influenza genes in mice.
Pla2g7 plays a crucial physiological role in smooth muscle cell differentiation from stem cells, and interactions between Nrf3 (show NFE2L3 Proteins) and Pla2g7 are essential.
The effects of a specific lp-PLA2 inhibitor on atherosclerosis in ApoE (show APOE Proteins)-deficient mice and its associated mechanisms, are reported.
Studies designed to evaluate the ability of precursor forms of PAF-AH to mature to fully active proteins indicated that the N-terminal end of human and mouse PAF-AH played important and opposite roles in this process.
The protein encoded by this gene is a secreted enzyme that catalyzes the degradation of platelet-activating factor to biologically inactive products. Defects in this gene are a cause of platelet-activating factor acetylhydrolase deficiency. Two transcript variants encoding the same protein have been found for this gene.
, 2-acetyl-1-alkylglycerophosphocholine esterase
, LDL-associated phospholipase A2
, PAF 2-acylhydrolase
, PAF acetylhydrolase
, group-VIIA phospholipase A2
, lipoprotein-associated phospholipase A2
, platelet-activating factor acetylhydrolase
, group VII phospholipase A2
, plasma PAF acetylhydrolase