Glucocorticoid receptors in human epicardial adipose tissue: Role of coronary status
A. Silaghi1, H. Silaghi2, T. Scridon3, R. Pais4, and V. Achard5
1County Emergency Hospital, Department of Endocrinology; 22nd Department of Surgery, University of Medicine and Pharmacy (Iuliu Hatieganu); 3Department of Cardiac Surgery, Cluj Heart Institute; 42nd Department of Internal Medicine, University of Medicine and Pharmacy (Iuliu Hatieganu), Cluj-Napoca, Romania; 5Infertility Care Unit, La Conception Hospital, Assistance Publique - Hopitaux de Marseille, Marseille, France

Background: Epicardial adipose tissue (EAT) is in close contact with coronary vessels and therefore could alter coronary homeostasis. Glucocorticoids are pathophysiological mediators of visceral fat deposition and its associated atherogenic complications. Aim: We investigated in EAT the expression of the glucocorticoid receptor (GR) and its various (A, B, C) promoters. Materials and methods: Paired subcutaneous adipose tissue (SAT) and EAT biopsies were obtained from 15 patients with coronary artery disease (CAD) and 12 patients without CAD (NCAD). GR and 11β-hydroxysteroid dehydrogenase type 1 protein (11β-HSD-1, the enzyme which converts inactive cortisone into active cortisol) were studied by immunohistochemistry and GR and its various promoters were studied by mRNA quantitative RT-PCR. Results: GR and 11β-HSD-1 protein were expressed in adipocytes, stromal areas, isolated stromal cells close to adipocytes, and blood vessels. Total GR mRNA levels did not differ in SAT obtained from NCAD or CAD patients and were decreased in EAT, irrespectively of the coronary status, with parallel changes in promoter B- and C-, but not promoter Aassociated transcripts. Total GR mRNA and adipocyte surface in EAT obtained from CAD patients were correlated negatively (p<0.035, r=0.39). Conclusions: Our findings demonstrate that in EAT, GR gene promoters could play a role in tissue-specific GR expression levels. EAT may be less sensitive to glucocorticoids than SAT, preventing the EAT mass development in CAD patients and suggesting a protective role on coronary homeostasis. (J. Endocrinol. Invest. 35: 649-654, 2012) ©2012, Editrice Kurtis

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