Vianello, Elena and Dozio, Elena and Bandera, Francesco and Froldi, Marco and Micaglio, Emanuele and Lamont, John and Tacchini, Lorenza and Schmitz, Gerd and Romanelli, Massimiliano Marco Corsi (2020) Correlative Study on Impaired Prostaglandin E2 Regulation in Epicardial Adipose Tissue and Its Role in Maladaptive Cardiac Remodeling via EPAC2 and ST2 Signaling in Overweight Cardiovascular Disease Subjects. INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 21 (2): 520. ISSN , 1422-0067
Full text not available from this repository. (Request a copy)Abstract
There is recent evidence that the dysfunctional responses of a peculiar visceral fat deposit known as epicardial adipose tissue (EAT) can directly promote cardiac enlargement in the case of obesity. Here, we observed a newer molecular pattern associated with LV dysfunction mediated by prostaglandin E2 (PGE(2)) deregulation in EAT in a cardiovascular disease (CVD) population. A series of 33 overweight CVD males were enrolled and their EAT thickness, LV mass, and volumes were measured by echocardiography. Blood, plasma, EAT, and SAT biopsies were collected for molecular and proteomic assays. Our data show that PGE(2) biosynthetic enzyme (PTGES-2) correlates with echocardiographic parameters of LV enlargement: LV diameters, LV end diastolic volume, and LV masses. Moreover, PTGES-2 is directly associated with EPAC2 gene (r = 0.70, p < 0.0001), known as a molecular inducer of ST2/IL-33 mediators involved in maladaptive heart remodelling. Furthermore, PGE(2) receptor 3 (PTEGER3) results are downregulated and its expression is inversely associated with ST2/IL-33 expression. Contrarily, PGE(2) receptor 4 (PTGER4) is upregulated in EAT and directly correlates with ST2 molecular expression. Our data suggest that excessive body fatness can shift the EAT transcriptome to a pro-tissue remodelling profile, may be driven by PGE(2) deregulation, with consequent promotion of EPAC2 and ST2 signalling.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | OXIDATIVE STRESS; OBESITY; INFLAMMATION; RECEPTOR; CELLS; IL-33; FAT; EP3; E-2; LIPOLYSIS; epicardial adipose tissue (EAT); prostaglandin E2 (PGE(2)); EP3 receptor; EP4 receptor; exchange protein directly activated by cAMP isoform 2 (EPAC2); stimulating growth factor 2 (ST2); interleukin(IL)-33; Cardiovascular Diseases (CVDs); fat mass |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Klinische Chemie und Laboratoriumsmedizin |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 06 Apr 2021 07:18 |
| Last Modified: | 06 Apr 2021 07:18 |
| URI: | https://pred.uni-regensburg.de/id/eprint/45374 |
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