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    Translating the microRNA signature of microvesicles derived from human coronary artery smooth muscle cells in patients with familial hypercholesterolemia and coronary artery disease

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    Authors
    de Gonzalo-Calvo, D.
    Cenarro, A.
    Garlaschelli, K.
    Pellegatta, F.
    Vilades, D.
    Nasarre, L.
    Camino-Lopez, S.
    Crespo, J.
    Carreras, F.
    Leta, R.
    Catapano, A.
    Norata, Giuseppe
    Civeira, F.
    Llorente-Cortes, V.
    Date
    2017
    Type
    Journal Article
    
    Metadata
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    Citation
    de Gonzalo-Calvo, D. and Cenarro, A. and Garlaschelli, K. and Pellegatta, F. and Vilades, D. and Nasarre, L. and Camino-Lopez, S. et al. 2017. Translating the microRNA signature of microvesicles derived from human coronary artery smooth muscle cells in patients with familial hypercholesterolemia and coronary artery disease. Journal of Molecular and Cellular Cardiology. 106: pp. 55-67.
    Source Title
    Journal of Molecular and Cellular Cardiology
    DOI
    10.1016/j.yjmcc.2017.03.005
    ISSN
    0022-2828
    School
    School of Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/55571
    Collection
    • Curtin Research Publications
    Abstract

    © 2017 Elsevier Ltd 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.

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