title: Endothelial glucocorticoid receptor suppresses atherogenesis--brief report.
abstract: OBJECTIVE
  The purpose of this study was to determine the role of the endothelial glucocorticoid receptor in the pathogenesis of atherosclerosis.
  
  
  RESULTS
  Control mice and mice lacking the endothelial glucocorticoid receptor were bred onto an Apoe knockout background and subjected to high-fat diet feeding for 12 weeks. Assessment of body weight and total cholesterol and triglycerides before and after the diet revealed no differences between the 2 groups of mice. However, mice lacking the endothelial glucocorticoid receptor developed more severe atherosclerotic lesions in the aorta, brachiocephalic artery, and aortic sinus, as well as a heightened inflammatory milieu as evidenced by increased macrophage recruitment in the lesions.
  
  
  CONCLUSIONS
  These data suggest that the endothelial glucocorticoid receptor is important for tonic inhibition of inflammation and limitation of atherosclerosis progression in this model.
authors: Department of Pediatrics, Yale University School of Medicine, New Haven, CT.
authors: Julie E
authors: JE
authors: Goodwin
authors: Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT.|Department of Internal Medicine (Cardiology), Yale University School of Medicine, New Haven, CT.
authors: Xinbo
authors: X
authors: Zhang
authors: Integrative Cell Signaling and Neurobiology of Metabolism Program, Section of Comparative Medicine, Yale University School of Medicine, New Haven, CT.|Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT.
authors: Noemi
authors: N
authors: Rotllan
authors: Department of Pediatrics, Yale University School of Medicine, New Haven, CT.
authors: Yan
authors: Y
authors: Feng
authors: Department of Pediatrics, Yale University School of Medicine, New Haven, CT.
authors: Han
authors: H
authors: Zhou
authors: Integrative Cell Signaling and Neurobiology of Metabolism Program, Section of Comparative Medicine, Yale University School of Medicine, New Haven, CT.|Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT.
authors: Carlos
authors: C
authors: Fernández-Hernando
authors: Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT.|Department of Internal Medicine (Cardiology), Yale University School of Medicine, New Haven, CT.
authors: Jun
authors: J
authors: Yu
authors: Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT.|Department of Pharmacology, Yale University School of Medicine, New Haven, CT.
authors: William C
authors: WC
authors: Sessa
mesh_terms: D000818:Animals; D001011:Aorta / Q000378:metabolism / Q000473:pathology; D001018:Aortic Diseases / Q000097:blood / Q000235:genetics / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D001057:Apolipoproteins E / Q000172:deficiency / Q000235:genetics; D050197:Atherosclerosis / Q000097:blood / Q000235:genetics / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D001835:Body Weight; D016122:Brachiocephalic Trunk / Q000378:metabolism / Q000473:pathology; D002784:Cholesterol / Q000097:blood; D059305:Diet, High-Fat; D004195:Disease Models, Animal; D042783:Endothelial Cells / Q000378:metabolism*; D005838:Genotype; D008264:Macrophages / Q000276:immunology; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010641:Phenotype; D011965:Receptors, Glucocorticoid / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D012720:Severity of Illness Index; D013997:Time Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D001057:Apolipoproteins E; C575863:NR3C1 protein, mouse; D011965:Receptors, Glucocorticoid; D014280:Triglycerides; D002784:Cholesterol
keywords: atherosclerosis; endothelium; glucocorticoid receptor