Ángel Fernández-Trasancos1, Rosa María Agra1,2,3, Jose María García-Acuña1,2,3, Ángel Luis Fernández2,4, José Ramón González-Juanatey1,2,3, Sonia Eiras1,2. 1. Cardiology Group, Health Research Institute, University Clinical Hospital of Santiago de Compostela, Santiago de Compostela, Spain. 2. CiberCV Madrid, Spain. 3. Department of Cardiology and Coronary Unit, University Clinical Hospital of Santiago de Compostela, Santiago de Compostela, Spain. 4. Department of Heart Surgery, University Clinical Hospital of Santiago de Compostela, Santiago de Compostela, Spain.
Abstract
OBJECTIVE: Epicardial adipose tissue (EAT) in coronary artery disease is insulin resistant and has a proinflammatory profile. This study examined the regulation of EAT by exogenous omentin and its consequence on vascular cells. METHODS: Stromal vascular cells (SC) of EAT and subcutaneous adipose tissue (SAT) from patients who underwent heart surgery were cultured and exposed to adipogenic factors with or without omentin. Proinflammatory cytokine regulation by omentin was analyzed in SC and mature adipocytes. Glucose uptake by EAT and SAT explants was determined after insulin, omentin, or combined treatment. Human vascular cells were exposed to secretomes of SC, with and without omentin treatment. Migration of smooth muscle cells and expression of adhesion molecules were determined by wound healing or real-time polymerase chain reaction, respectively. RESULTS: Omentin treatment raised adipogenesis-induced adiponectin levels on SC of EAT and reduced TNF-α expression levels (0.58 ± 0.14-fold change; P = 0.034) in mature adipocytes. Omentin improved the insulin activity of EAT and SAT explants from cardiovascular disease patients. Finally, secretomes of SC under omentin treatment reduced the migration of smooth muscle cells. CONCLUSIONS: Exogenous omentin might support a cardioprotective role through its effect on EAT regarding glucose uptake, anti-inflammatory response, and its paracrine role on smooth muscle cells.
OBJECTIVE: Epicardial adipose tissue (EAT) in coronary artery disease is insulin resistant and has a proinflammatory profile. This study examined the regulation of EAT by exogenous omentin and its consequence on vascular cells. METHODS: Stromal vascular cells (SC) of EAT and subcutaneous adipose tissue (SAT) from patients who underwent heart surgery were cultured and exposed to adipogenic factors with or without omentin. Proinflammatory cytokine regulation by omentin was analyzed in SC and mature adipocytes. Glucose uptake by EAT and SAT explants was determined after insulin, omentin, or combined treatment. Human vascular cells were exposed to secretomes of SC, with and without omentin treatment. Migration of smooth muscle cells and expression of adhesion molecules were determined by wound healing or real-time polymerase chain reaction, respectively. RESULTS:Omentin treatment raised adipogenesis-induced adiponectin levels on SC of EAT and reduced TNF-α expression levels (0.58 ± 0.14-fold change; P = 0.034) in mature adipocytes. Omentin improved the insulin activity of EAT and SAT explants from cardiovascular diseasepatients. Finally, secretomes of SC under omentin treatment reduced the migration of smooth muscle cells. CONCLUSIONS: Exogenous omentin might support a cardioprotective role through its effect on EAT regarding glucose uptake, anti-inflammatory response, and its paracrine role on smooth muscle cells.
Authors: Rosa M Agra-Bermejo; Rocio Gonzalez-Ferreiro; J Nicolos Lopez-Canoa; Alfonso Varela-Roman; Ines Gomez-Otero; Sonia Eiras; José R González-Juanatey Journal: J Cardiovasc Transl Res Date: 2018-10-23 Impact factor: 4.132