Asprosin inhibits macrophage lipid accumulation and reduces atherosclerotic burden by up-regulating ABCA1 and ABCG1 expression via the p38/Elk-1 pathway.

ABSTRACT:

Background

Asprosin, a newly discovered adipokine, is a C-terminal cleavage product of profibrillin. Asprosin has been reported to participate in lipid metabolism and cardiovascular disease, but its role in atherogenesis remains elusive.

Methods

Asprosin was overexpressed in THP-1 macrophage-derived foam cells and apoE^-/- mice using the lentiviral vector. The expression of relevant molecules was determined by qRT-PCR and/or western blot. The intracellular lipid accumulation was evaluated by high-performance liquid chromatography and Oil red O staining. HE and Oil red O staining was employed to assess plaque burden in vivo. Reverse cholesterol transport (RCT) efficiency was measured using [³H]-labeled cholesterol.

Results

Exposure of THP-1 macroph

SUBMITTER: Zou J 

PROVIDER: S-EPMC9331044 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature