Abstract
Leukocyte cell-derived chemotaxin 2 (LECT2), a multifunctional hepatokine, is involved in many pathological conditions. However, its role in atherosclerosis remains undefined. In this study, we administered vehicle or LECT2 to male Apoe-/- mice fed a Western diet for 15 weeks. Atherosclerotic lesions were visualized and quantified with Oil-red O and hematoxylin staining. The mRNA expression levels of MCP-1, MMP-1, IL-8, IL-1β, and TNF-α were analyzed by quantitative real-time polymerase chain reaction. Serum TNF-α, IL-1β, IL-8, MCP-1, and MMP-1 concentrations were measured by enzyme-linked immunosorbent assay. CD68, CD31, and α-SMA, markers of macrophages, endothelial cells, and smooth muscle cells, respectively, were detected by immunostaining. Results showed that LECT2 reduced total cholesterol and low-density lipoprotein concentrations in serum and inhibited the development of atherosclerotic lesions, accompanied by reductions in inflammatory cytokines and lower MCP-1, MMP-1, TNF-α, IL-8, and IL-1β mRNA abundance. Furthermore, LECT2 decreased CD68, but increased α-SMA in atherosclerotic lesions, suggesting an increase in smooth muscle cells and reduction in macrophages. In summary, LECT2 inhibited the development of atherosclerosis in mice, accompanied by reduced serum total cholesterol concentration and lower inflammatory responses.
Highlights
Cardiovascular diseases are the leading cause of mortality worldwide
Leukocyte cell-derived chemotaxin 2 (LECT2) inhibited development of atherosclerotic lesions in Apoe– / – mice We analyzed the levels of LECT2 in the AS and control groups to examine the relationship between serum LECT2 levels and atherosclerosis
The LECT2 group had less atherosclerotic plaque in the ascending aortic arch and thoracic regions compared with the AS group (P
Summary
Cardiovascular diseases are the leading cause of mortality worldwide. With ageing populations and increasing exposure to metabolic risks, deaths due to cardiovascular diseases will increase to approximately 23 million by 2030 (GBD 2017 Risk Factor Collaborators, 2018). Atherosclerosis is an important underlying cause of many clinical cardiovascular events, and is a systemic disease characterized by fatty deposits, in flammation, cell death, fibrosis, and scar tissue build up within the walls of arteries (Mozaffarian et al, 2016). Vascular smooth muscle cells (VSMCs) migrate from the media to intima, and proliferate and produce extracellular matrix to form a fibrous cap that covers atherosclerotic plaque (Allahverdian et al, 2018). During this stage, the secretion of many proinflammatory cytokines is increased, including interleukin (IL)-8, IL-1 β , monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor (TNF)-α (Chistiakov et al, 2015). The precise pathogenesis of atherosclerosis has not been clarified, it is widely accepted that inflammation and lipid disorder both play crucial roles
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