title: Enhanced expression of salusin-β contributes to progression of atherosclerosis in LDL receptor deficient mice.
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.
authors.affiliation: Department of Pharmacology, Xuzhou Medical College, Xuzhou, P.R. China.
authors.forename: Cheng-Hua
authors.initials: CH
authors.lastname: Zhou
authors.forename: Lan-Lan
authors.initials: LL
authors.lastname: Liu
authors.forename: Yu-Qing
authors.initials: YQ
authors.lastname: Wu
authors.forename: Zheng
authors.initials: Z
authors.lastname: Song
authors.forename: Shu-Hua
authors.initials: SH
authors.lastname: Xing
mesh_terms: D000818:Animals; D001158:Arteries / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D050197:Atherosclerosis / Q000097:blood / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D002784:Cholesterol / Q000097:blood; D004195:Disease Models, Animal; D018450:Disease Progression; D005786:Gene Expression Regulation / Q000187:drug effects / Q000235:genetics*; D036341:Intercellular Signaling Peptides and Proteins / Q000096:biosynthesis* / Q000494:pharmacology; D050356:Lipid Metabolism / Q000187:drug effects / Q000502:physiology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D058226:Plaque, Atherosclerotic / Q000139:chemically induced / Q000473:pathology; D011498:Protein Precursors / Q000096:biosynthesis* / Q000494:pharmacology; D011973:Receptors, LDL / Q000235:genetics*
chemical_list: D036341:Intercellular Signaling Peptides and Proteins; D011498:Protein Precursors; D011973:Receptors, LDL; D002784:Cholesterol