Enhanced expression of salusin-β contributes to progression of atherosclerosis in LDL receptor deficient mice.

Atherosclerosis is an important underlying pathology of cardiovascular diseases. The aim of this study was to observe the expression of salusin-β, a new vasoactive peptide, in vascular tissues of low-density lipoprotein receptor deficient (LDLR(-/-)) mice, and to evaluate the effect of salusin-β on the development of atherosclerosis in LDLR(-/-) mice. Six-week-old, male LDLR(-/-) mice were subcutaneously injected with salusin-β or the vehicle, once a day for 12 weeks. The expressions of salusin-β in both mRNA and peptide levels were determined by reverse transcription - polymerase chain reaction, Western blot, and immunohistochemistry. Atherosclerotic lesions were analyzed by staining with hematoxylin and eosin or oil red O. Our results showed that expression of salusin-β in mRNA and salusin-β peptide levels were enhanced in LDLR(-/-) mice. Subcutaneous injection of salusin-β significantly aggravated the atherosclerotic lesions, and increased lipid deposits in the arteries of LDLR(-/-) mice. Moreover, salusin-β significantly increased the serum level of low-density lipoprotein cholesterol, but not total cholesterol, triglycerides, or high-density lipoprotein cholesterol. These results suggest that the enhanced expression of salusin-β contributes to progression of atherosclerosis in LDLR(-/-) mice by up-regulating the serum low-density lipoprotein cholesterol level. This study provides a potential therapeutic target for the prevention and treatment of atherosclerosis.