Human Neutrophil Peptide 1 Limits Hypercholesterolemia-induced Atherosclerosis by Increasing Hepatic LDL Clearance.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 28111237.
- Also identified by DOI 10.1016/j.ebiom.2017.01.006 and PMC identifier 5474437.
- Licence recorded as CC BY-NC-ND.
- Because redistribution is not established, this page shows the abstract only. Follow the links below for the full text.
Abstract
Increases in plasma LDL-cholesterol have unequivocally been established as a causal risk factor for atherosclerosis. Hence, strategies for lowering of LDL-cholesterol may have immediate therapeutic relevance. Here we study the role of human neutrophil peptide 1 (HNP1) in a mouse model of atherosclerosis and identify its potent atheroprotective effect both upon transgenic overexpression and therapeutic delivery. The effect was found to be due to a reduction of plasma LDL-cholesterol. Mechanistically, HNP1 binds to apolipoproteins enriched in LDL. This interaction facilitates clearance of LDL particles in the liver via LDL receptor. Thus, we here identify a non-redundant mechanism by which HNP1 allows for reduction of LDL-cholesterol, a process that may be therapeutically instructed to lower cardiovascular risk.
Medical subject headings
- Atherosclerosis
- Hypercholesterolemia
- Lipoproteins, LDL
- Liver
- alpha-Defensins