title: Increased IL-37 in Atherosclerotic Disease could be Suppressed by Atorvastatin Therapy.
abstract: Recently, the evidence showed that interleukin-37 (IL-37) was expressed in the foam-like cells of atherosclerotic coronary and carotid artery plaques in IL-37-transgenic mice, suggesting that interleukin-37 is involved in atherosclerosis-related diseases. The purpose of this study was to determine the change of IL-37 in atherosclerotic plaque, the effect of atorvastatin on IL-37 and the association between IL-37 and Smad3 in atherosclerotic disease. Rabbits were subjected to atherosclerosis by the immunologic injury composite with balloon injury (BI). Some rabbits received atorvastatin treatment from 6 weeks to 12 weeks. Serum levels of IL-37 were assessed at baseline, 6 weeks and 12 weeks in normal, atherosclerotic and atorvastatin groups. Protein and RNA levels of IL-37 atherosclerotic plaque from abdominal aorta were processed at 12 weeks. Abdominal aorta including atherosclerotic plaque was immunostained with IL-37 and Smad3. Serum IL-37 significantly increased in atherosclerotic disease, and this increase could be reduced by the atorvastatin treatment. IL-37 and Smad3 were accumulated in the macrophage-derived foam cells in the plaque and significantly increased in protein and RNA levels. Atorvastatin treatment could significantly suppress the increase of both IL-37 and Smad3. Plasma level of IL-37 and the IL-37 expression of the plaque were significantly increased in atherosclerotic disease. This increase could be suppressed by the atorvastatin treatment. In addition, Smad3 might be required for IL-37 activity during the atherosclerotic physiologic process.
authors.affiliation: Department of cardiology, Nanshan Hospital, Guangdong Medical College, Shenzhen, China.
authors.forename: C
authors.initials: C
authors.lastname: Shaoyuan
authors.affiliation: Department of Pathophysiology, School of Medicine, Shenzhen University, Shenzhen, China.
authors.forename: D
authors.initials: D
authors.lastname: Ming
authors.affiliation: School of Guangdong Medical College, Zhanjiang, China.
authors.forename: H
authors.initials: H
authors.lastname: Yulang
authors.affiliation: Department of cardiology, Nanshan Hospital, Guangdong Medical College, Shenzhen, China.
authors.forename: F
authors.initials: F
authors.lastname: Hongcheng
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000188:drug therapy* / Q000276:immunology; D000069059:Atorvastatin / Q000627:therapeutic use*; D005487:Foam Cells / Q000276:immunology; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D007375:Interleukin-1 / Q000037:antagonists & inhibitors* / Q000097:blood / Q000276:immunology; D008297:Male; D058226:Plaque, Atherosclerotic / Q000188:drug therapy / Q000276:immunology; D012333:RNA, Messenger / Q000235:genetics; D011817:Rabbits; D051900:Smad3 Protein / Q000378:metabolism
chemical_list: D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007375:Interleukin-1; D012333:RNA, Messenger; D051900:Smad3 Protein; D000069059:Atorvastatin