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Title: Enhanced expression of salusin-β contributes to progression of atherosclerosis in LDL receptor deficient mice. Author: Zhou CH, Liu LL, Wu YQ, Song Z, Xing SH. Journal: Can J Physiol Pharmacol; 2012 Apr; 90(4):463-71. PubMed ID: 22462492. Abstract: 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.[Abstract] [Full Text] [Related] [New Search]