Adipokine Chemerin Stimulates Progression of Atherosclerosis in ApoE−− Mice

Abstract EN

Background.

Vascular remodeling is the most critical pathogenesis of atherosclerosis.

Adipokine chemerin was known for its relationship with obesity as well as metabolism.

Most recently, chemerin was found to play a crucial role in the pathologic process of cardiovascular diseases including coronary heart disease.

In this study, we surveyed the role of chemerin in progression of atherosclerosis in ApoE−/− mice.

Objective.

To investigate the relationship between chemerin and progression of atherosclerosis in ApoE−/− mice and its mechanism.

Methods.

8-week-old ApoE−/− mice were fed with high-fat diet to induce the atherosclerosis model.

Adenoviruses were transfected for knockdown or overexpression of chemerin gene into aorta.

Serums and aortic tissues of ApoE−/− mice were obtained after feeding high-fat diet for 16 weeks.

HE staining and oil red staining were performed to evaluate aortic plaque.

ELISA was performed to explore serum levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and transforming growth factor-β1 (TGF-β1).

Real-time PCR and western blotting were carried out to investigate the mRNA and protein levels of chemerin, nuclear factor-κB p65 (NF-κBp65), proliferating cell nuclear antigen (PCNA), phosphorylated p38 mitogen-activated protein kinase (p-p38-MAPK), phosphorylated c-Jun N-terminal kinase (p-JNK), and phosphorylated extracellular signal regulated kinase 1/2 (p-ERK 1/2).

Result.

Aortic plaque formation was significantly induced by high-fat diet in ApoE−/− mice.

Simultaneously, elevated serum levels of TNF-α and IL-1β and elevated mRNA and protein levels of chemerin, NF-κBp65, PCNA, p-p38-MAPK, p-JNK, and p-ERK 1/2 were found in ApoE−/− mice.

After aortic chemerin gene was inhibited by adenovirus, aortic atherosclerosis induced by high-fat diet was significantly meliorated, serum levels of TNF-α and IL-1β decreased, mRNA and protein levels of NF-κBp65, PCNA, p-p38-MAPK, p-JNK, and p-ERK 1/2 decreased simultaneously.

Conclusion.

Our study revealed that chemerin stimulated the progression of atherosclerosis in ApoE−/− mice.