Abstract
Atherosclerosis is an inflammatory disease with fundamental primitive events including endothelial dysfunction and platelet aggregation [1]. Human neutrophil peptides (HNP) are the most abundant cationic proteins in neutrophils and are released into the extracellular milieu upon activation [2]. HNP have previously been detected in atherosclerotic lesions, and are in high concentrations in blood of patients with acute coronary syndrome [2]. We have previously demonstrated that HNP can induce foam cell formation, platelet aggregation and leukocyte recruitment through the LRP8 signaling pathway [3], but there is no direct interaction between HNP and LRP8.
Highlights
Atherosclerosis is an inflammatory disease with fundamental primitive events including endothelial dysfunction and platelet aggregation [1]
We have previously demonstrated that Human neutrophil peptides (HNP) can induce foam cell formation, platelet aggregation and leukocyte recruitment through the LRP8 signaling pathway [3], but there is no direct interaction between HNP and LRP8
We examined if HNP-induced endothelial dysfunction and platelet aggregation through the LRP8-signaling pathway is mediated by the LRP ligand reelin
Summary
Atherosclerosis is an inflammatory disease with fundamental primitive events including endothelial dysfunction and platelet aggregation [1]. Human neutrophil peptides (HNP) are the most abundant cationic proteins in neutrophils and are released into the extracellular milieu upon activation [2]. HNP have previously been detected in atherosclerotic lesions, and are in high concentrations in blood of patients with acute coronary syndrome [2]. We have previously demonstrated that HNP can induce foam cell formation, platelet aggregation and leukocyte recruitment through the LRP8 signaling pathway [3], but there is no direct interaction between HNP and LRP8
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