Lp-PLA2 et sPLA2

Ait‐Oufella, Hafid; Mallat, Ziad; Tedgui, Alain

doi:10.1051/medsci/20143005015

Cited by 9 publications

(2 citation statements)

References 37 publications

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“…Phospholipases A2 are part of a superfamily of enzymes responsible for catalysing glycerophospholipids' hydrolysis [126]. sPLA2V inhibited the generation and anti-apoptotic effects of APC by binding to EPCR on the endothelial cells (Figure 4) [127,128].…”

Section: Secretory Group V Phospholipases A2 (Spla2v)mentioning

confidence: 99%

Endothelial Protein C Receptor and Its Impact on Rheumatic Disease

O’Hehir,

Lynch,

O’Neill

et al. 2024

JCM

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Endothelial Protein C Receptor (EPCR) is a key regulator of the activated protein C anti-coagulation pathway due to its role in the binding and activation of this protein. EPCR also binds to other ligands such as Factor VII and X, γδ T-cells, plasmodium falciparum erythrocyte membrane protein 1, and Secretory group V Phospholipases A2, facilitating ligand-specific functions. The functions of EPCR can also be regulated by soluble (s)EPCR that competes for the binding sites of membrane-bound (m)EPCR. sEPCR is created when mEPCR is shed from the cell surface. The propensity of shedding alters depending on the genetic haplotype of the EPCR gene that an individual may possess. EPCR plays an active role in normal homeostasis, anti-coagulation pathways, inflammation, and cell stemness. Due to these properties, EPCR is considered a potential effector/mediator of inflammatory diseases. Rheumatic diseases such as rheumatoid arthritis and systemic lupus erythematosus are autoimmune/inflammatory conditions that are associated with elevated EPCR levels and disease activity, potentially driven by EPCR. This review highlights the functions of EPCR and its contribution to rheumatic diseases.

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Section: Secretory Group V Phospholipases A2 (Spla2v)mentioning

confidence: 99%

Endothelial Protein C Receptor and Its Impact on Rheumatic Disease

O’Hehir,

Lynch,

O’Neill

et al. 2024

JCM

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“…Many experimental studies have shown that PLA2 is involved in lipid metabolism and immunoinflammatory response and participates in the development of atherosclerosis. 12 13 Darapladib is an oral, investigational, highly potent, and selective Lp-PLA2 inhibitor.…”

Section: Introductionmentioning

confidence: 99%

Darapladib, a Lipoprotein-Associated Phospholipase A2 Inhibitor, Reduces Rho Kinase Activity in Atherosclerosis

Zhang

Liu³

et al. 2016

Yonsei Med J

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PurposeIncreased lipoprotein-associated phospholipase A2 (Lp-PLA2) activity and Rho kinase activity may be associated with atherosclerosis. The principal aim of this study was to examine whether darapladib (a selective Lp-PLA2 inhibitor) could reduce the elevated Lp-PLA2 and Rho kinase activity in atherosclerosis.Materials and MethodsStudies were performed in male Sprague-Dawley rats. The atherosclerosis rats were prepared by feeding them with a high-cholesterol diet for 10 weeks. Low-dose darapladib (25 mg·kg-1·d-1) and high-dose darapladib (50 mg·kg-1·d-1) interventions were then administered over the course of 2 weeks.ResultsThe serum levels of triglycerides, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), high-sensitivity C-reactive protein (hs-CRP), and Lp-PLA2, significantly increased in atherosclerosis model groups, as did Rho kinase activity and cardiomyocyte apoptosis (p<0.05 vs. sham group), whereas nitric oxide (NO) production was reduced. Levels of TC, LDL-C, CRP, Lp-PLA2, and Rho kinase activity were respectively reduced in darapladib groups, whereas NO production was enhanced. When compared to the low-dose darapladib group, the reduction of the levels of TC, LDL-C, CRP, and Lp-PLA2 was more prominent in the high-dose darapladib group (p<0.05), and the increase of NO production was more prominent (p<0.05). Cardiomyocyte apoptosis of the high-dose darapladib group was also significantly reduced compared to the low-dose darapladib group (p<0.05). However, there was no significant difference in Rho kinase activity between the low-dose darapladib group and the high-dose darapladib group (p>0.05).ConclusionDarapladib, a Lp-PLA2 inhibitor, leads to cardiovascular protection that might be mediated by its inhibition of both Rho kinase and Lp-PLA2 in atherosclerosis.

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2018

Cardiovascular Disease

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Lp-PLA2 et sPLA2

Cited by 9 publications

References 37 publications

Endothelial Protein C Receptor and Its Impact on Rheumatic Disease

Endothelial Protein C Receptor and Its Impact on Rheumatic Disease

Darapladib, a Lipoprotein-Associated Phospholipase A2 Inhibitor, Reduces Rho Kinase Activity in Atherosclerosis

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