Institute of Biomedical Research of Barcelona IIBB Spanish National Research Council CSIC

Barcelona, Spain

Institute of Biomedical Research of Barcelona IIBB Spanish National Research Council CSIC

Barcelona, Spain
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de Gonzalo-Calvo D.,Biomedical Research Institute Sant Pau | de Gonzalo-Calvo D.,Institute Salud Carlos III | Cenarro A.,Institute Salud Carlos III | Cenarro A.,University of Zaragoza | And 19 more authors.
Journal of Molecular and Cellular Cardiology | Year: 2017

Aims: To analyze the impact of atherogenic lipoproteins on the miRNA signature of microvesicles derived from human coronary artery smooth muscle cells (CASMC) and to translate these results to familial hypercholesterolemia (FH) and coronary artery disease (CAD) patients. Methods: Conditioned media was collected after exposure of CASMC to atherogenic lipoproteins. Plasma samples were collected from two independent populations of diagnosed FH patients and matched normocholesterolemic controls (Study population 1, N = 50; Study population 2, N = 24) and a population of patients with suspected CAD (Study population 3, N = 50). Extracellular vesicles were isolated and characterized using standard techniques. A panel of 30 miRNAs related to vascular smooth muscle cell (VSMC) (patho-)physiology was analyzed using RT-qPCR. Results: Atherogenic lipoproteins significantly reduced levels of miR-15b-5p, − 24-3p, − 29b-3p, − 130a-3p, − 143-3p, − 146a-3p, − 222-3p, − 663a levels (P < 0.050) in microvesicles (0.1 μm–1 μm in diameter) released by CASMC. Two of these miRNAs, miR-24-3p and miR-130a-3p, were reduced in circulating microvesicles from FH patients compared with normocholesterolemic controls in a pilot study (Study population 1) and in different validation studies (Study populations 1 and 2) (P < 0.050). Supporting these results, plasma levels of miR-24-3p and miR-130a-3p were also downregulated in FH patients compared to controls (P < 0.050). In addition, plasma levels of miR-130a-3p were inversely associated with coronary atherosclerosis in a cohort of suspected CAD patients (Study population 3) (P < 0.050). Conclusions: Exposure to atherogenic lipoproteins modifies the miRNA profile of CASMC-derived microvesicles and these alterations are reflected in patients with FH. Circulating miR-130a-3p emerges as a potential biomarker for coronary atherosclerosis. © 2017 Elsevier Ltd


Samouillan V.,CNRS Inter-university Material Research and Engineering | Revuelta-Lopez E.,Hospital Of La Santa Creu I Sant Pau | Soler-Botija C.,Institute Salud Carlos III | Dandurand J.,CNRS Inter-university Material Research and Engineering | And 11 more authors.
Biochimica et Biophysica Acta - Molecular Basis of Disease | Year: 2017

Adverse cardiac remodeling after myocardial infarction (MI) causes impaired ventricular function and heart failure. Histopathological characterization is commonly used to detect the location, size and shape of MI sites. However, the information about chemical composition, physical structure and molecular mobility of peri- and infarct zones post-MI is rather limited. The main objective of this work was to explore the spatiotemporal biochemical and biophysical alterations of key cardiac components post-MI. The FTIR spectra of healthy and remote myocardial tissue shows amides A, I, II and III associated with proteins in freeze-died tissue as major absorptions bands. In infarcted myocardium, the spectrum of these main absorptions was deeply altered. FITR evidenced an increase of the amide A band and the distinct feature of the collagen specific absorption band at 1338 cm− 1 in the infarct area at 21 days post-MI. At 21 days post-MI, it also appears an important shift of amide I from 1646 cm− 1 to 1637 cm− 1 that suggests the predominance of the triple helical conformation in the proteins. The new spectra bands also indicate an increase in proteoglycans, residues of carbohydrates in proteins and polysaccharides in ischemic areas. Thermal analysis indicates a deep increase of unfreezable water/freezable water in peri- and infarcted tissues. In infarcted tissue is evidenced the impairment of myofibrillar proteins thermal profile and the emergence of a new structure. In conclusion, our results indicate a profound evolution of protein secondary structures in association with collagen deposition and reorganization of water involved in the scar maturation of peri- and infarct zones post-MI. © 2017 Elsevier B.V.

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