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101. Genome-wide profiling of the cardiac transcriptome after myocardial infarction identifies novel heart-specific long non-coding RNAs

Author

Ounzain, S., primary, Micheletti, R., additional, Beckmann, T., additional, Schroen, B., additional, Alexanian, M., additional, Pezzuto, I., additional, Crippa, S., additional, Nemir, M., additional, Sarre, A., additional, Johnson, R., additional, Dauvillier, J., additional, Burdet, F., additional, Ibberson, M., additional, Guigo, R., additional, Xenarios, I., additional, Heymans, S., additional, and Pedrazzini, T., additional

Published
2014
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103. A deep sequencing approach to uncover the miRNOME in the human heart

Author

Leptidis, S., el Azzouzi, H., Lok, S.I., de Weger, R., Olieslagers, S., Kisters, N., Silva, G.J., Heymans, S., Cuppen, E., Berezikov, E., de Windt, L.J., da Costa Martins, P., Leptidis, S., el Azzouzi, H., Lok, S.I., de Weger, R., Olieslagers, S., Kisters, N., Silva, G.J., Heymans, S., Cuppen, E., Berezikov, E., de Windt, L.J., and da Costa Martins, P.

Abstract

MicroRNAs (miRNAs) are a class of non-coding RNAs of approximately 22 nucleotides in length, and constitute a novel class of gene regulators by imperfect base-pairing to the 3'UTR of protein encoding messenger RNAs. Growing evidence indicates that miRNAs are implicated in several pathological processes in myocardial disease. The past years, we have witnessed several profiling attempts using high-density oligonucleotide array-based approaches to identify the complete miRNA content (miRNOME) in the healthy and diseased mammalian heart. These efforts have demonstrated that the failing heart displays differential expression of several dozens of miRNAs. While the total number of experimentally validated human miRNAs is roughly two thousand, the number of expressed miRNAs in the human myocardium remains elusive. Our objective was to perform an unbiased assay to identify the miRNOME of the human heart, both under physiological and pathophysiological conditions. We used deep sequencing and bioinformatics to annotate and quantify microRNA expression in healthy and diseased human heart (heart failure secondary to hypertrophic or dilated cardiomyopathy). Our results indicate that the human heart expresses >800 miRNAs, the majority of which not being annotated nor described so far and some of which being unique to primate species. Furthermore, >250 miRNAs show differential and etiology-dependent expression in human dilated cardiomyopathy (DCM) or hypertrophic cardiomyopathy (HCM). The human cardiac miRNOME still possesses a large number of miRNAs that remain virtually unexplored. The current study provides a starting point for a more comprehensive understanding of the role of miRNAs in regulating human heart disease., MicroRNAs (miRNAs) are a class of non-coding RNAs of approximately 22 nucleotides in length, and constitute a novel class of gene regulators by imperfect base-pairing to the 3'UTR of protein encoding messenger RNAs. Growing evidence indicates that miRNAs are implicated in several pathological processes in myocardial disease. The past years, we have witnessed several profiling attempts using high-density oligonucleotide array-based approaches to identify the complete miRNA content (miRNOME) in the healthy and diseased mammalian heart. These efforts have demonstrated that the failing heart displays differential expression of several dozens of miRNAs. While the total number of experimentally validated human miRNAs is roughly two thousand, the number of expressed miRNAs in the human myocardium remains elusive. Our objective was to perform an unbiased assay to identify the miRNOME of the human heart, both under physiological and pathophysiological conditions. We used deep sequencing and bioinformatics to annotate and quantify microRNA expression in healthy and diseased human heart (heart failure secondary to hypertrophic or dilated cardiomyopathy). Our results indicate that the human heart expresses >800 miRNAs, the majority of which not being annotated nor described so far and some of which being unique to primate species. Furthermore, >250 miRNAs show differential and etiology-dependent expression in human dilated cardiomyopathy (DCM) or hypertrophic cardiomyopathy (HCM). The human cardiac miRNOME still possesses a large number of miRNAs that remain virtually unexplored. The current study provides a starting point for a more comprehensive understanding of the role of miRNAs in regulating human heart disease.

Published
2013

111. Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases

Author

Caforio, A. L. P., primary, Pankuweit, S., additional, Arbustini, E., additional, Basso, C., additional, Gimeno-Blanes, J., additional, Felix, S. B., additional, Fu, M., additional, Helio, T., additional, Heymans, S., additional, Jahns, R., additional, Klingel, K., additional, Linhart, A., additional, Maisch, B., additional, McKenna, W., additional, Mogensen, J., additional, Pinto, Y. M., additional, Ristic, A., additional, Schultheiss, H.-P., additional, Seggewiss, H., additional, Tavazzi, L., additional, Thiene, G., additional, Yilmaz, A., additional, Charron, P., additional, and Elliott, P. M., additional

Published
2013
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112. Using Prolog as the Fundament for Applications on the Semantic Web

Author

Polleres, A., Pearce, D., Heymans, S., Ruckhaus, E., Wielemaker, J. (Jan), Hildebrand, M. (Michiel), Ossenbruggen, J.R. (Jacco) van, Polleres, A., Pearce, D., Heymans, S., Ruckhaus, E., Wielemaker, J. (Jan), Hildebrand, M. (Michiel), and Ossenbruggen, J.R. (Jacco) van

Abstract

This article describes the experiences developing a Semantic Web application entirely in Prolog. The application, a demonstrator that provides access to multiple art collections and linking these using cultural heritage vocabula

Published
2007

115. Oral abstract presentations & Young Investigators Competition

Author

Leone, A., primary, Aquila, I., additional, Vicinanza, C., additional, Iaconetti, C., additional, Bochicchio, A., additional, Ottolenghi, S., additional, Indolfi, C., additional, Nadal-Ginard, B., additional, Ellison, G. M., additional, Torella, D., additional, Mias, C., additional, Genet, G., additional, Guilbeau-Frugier, C., additional, Pathak, A., additional, Senard, J. M., additional, Gales, C., additional, Egorova, A. D., additional, Khedoe, P. S. J., additional, Goumans, M. T. H., additional, Nauli, S. M., additional, Ten Dijke, P., additional, Poelmann, R. E., additional, Hierck, B. P., additional, Miragoli, M., additional, Lab, M. J., additional, Singh, A., additional, Sikkel, M., additional, Lyon, A., additional, Gorelik, J., additional, Cheung, C., additional, Bernardo, A. S., additional, Trotter, M. W., additional, Pedersen, R. A., additional, Sinha, S., additional, Mioulane, M., additional, Foldes, G., additional, Harding, S. E., additional, Reglin, B., additional, Secomb, T. W., additional, Pries, A. R., additional, Buckingham, M., additional, Lescroart, F., additional, Meilhac, S., additional, Le Garrec, J.-F., additional, Rozmaritsa, N., additional, Christ, T., additional, Wettwer, E., additional, Knaut, M., additional, Ravens, U., additional, Tokar, S., additional, Schobesberger, S., additional, Wright, P. T., additional, Lyon, A. R., additional, Van Mil, A., additional, Grundmann, S., additional, Goumans, M.-J., additional, Jaksani, S., additional, Doevendans, P. A., additional, Sluijter, J. P., additional, Tijsen, A. J., additional, Amin, A. S., additional, Giudicessi, J. R., additional, Tanck, M. W., additional, Bezzina, C. R., additional, Creemers, E. E., additional, Wilde, A. M., additional, Ackerman, M. J., additional, Pinto, Y. M., additional, Gedicke-Hornung, C., additional, Behrens-Gawlik, V., additional, Khajetoorians, D., additional, Mearini, G., additional, Reischmann, S., additional, Geertz, B., additional, Voit, T., additional, Dreyfus, P., additional, Eschenhagen, T., additional, Carrier, L., additional, Duerr, G. D., additional, Heinemann, J. C., additional, Wenzel, D., additional, Ghanem, A., additional, Alferink, J. C., additional, Zimmer, A., additional, Lutz, B., additional, Welz, A., additional, Fleischmann, B. K., additional, Dewald, O., additional, Sbroggio', M., additional, Bertero, A., additional, Giuliano, L., additional, Brancaccio, M., additional, Tarone, G., additional, Meiser, M., additional, Kohlhaas, M., additional, Chen, Y., additional, Csordas, G., additional, Dorn, G., additional, Maack, C., additional, Stapel, B., additional, Hoch, M., additional, Haghikia, A., additional, Fischer, P., additional, Hilfiker-Kleiner, D., additional, Schroen, B., additional, Corsten, M., additional, Verhesen, W., additional, De Windt, L., additional, Zacchigna, S., additional, Thum, T., additional, Carmeliet, P., additional, Papageorgiou, A., additional, Heymans, S., additional, Lunde, I. G., additional, Finsen, A. V., additional, Florholmen, G., additional, Skrbic, B., additional, Kvaloy, H., additional, Jarstadmarken, H. O., additional, Sjaastad, I., additional, Tonnessen, T., additional, Carlson, C. R., additional, Christensen, G., additional, Paavola, J., additional, Schliffke, S., additional, Rossetti, S., additional, Kuo, I., additional, Yuan, S., additional, Sun, Z., additional, Harris, P., additional, Torres, V., additional, Ehrlich, B., additional, Robinson, P., additional, Adams, K., additional, Zhang, Y.-H., additional, Casadei, B., additional, Watkins, H., additional, Redwood, C., additional, Seneviratne, A. N., additional, Cole, J. E., additional, Goddard, M. E., additional, Mohri, Z., additional, Cross, A. J., additional, Krams, R., additional, Monaco, C., additional, Everaert, B. R., additional, Van Laere, S. J., additional, Hoymans, V. Y., additional, Timmermans, J. P., additional, and Vrints, C. J., additional

Published
2012
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116. Thrombospondin-2 prevents cardiac injury and dysfunction in viral myocarditis through the activation of regulatory T-cells

Author

Papageorgiou, A.-P., primary, Swinnen, M., additional, Vanhoutte, D., additional, VandenDriessche, T., additional, Chuah, M., additional, Lindner, D., additional, Verhesen, W., additional, de Vries, B., additional, D'hooge, J., additional, Lutgens, E., additional, Westermann, D., additional, Carmeliet, P., additional, and Heymans, S., additional

Published
2012
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141. Inflammation and Cardiac Remodeling During Viral Myocarditis.

Author

Stock, G., Lessl, M., Schultheiss, H. -P., Kapp, J. -F., Grötzbach, G., and Heymans, S.

Abstract

Acute viral myocarditis is the main cause of cardiac failure in young patients and accounts for up to 60% of "idiopathic" dilated cardiomyopathy. The clinical course of viral myocarditis is mostly insidious with limited cardiac inflammation and dysfunction. However, overwhelming inflammation may occur in a subset of patients, leading to fulminant cardiac injury, whereas others develop chronic heart failure due to autoimmune myocarditis. Today, little effective treatment exists for patients, apart from general supportive therapy and antifailure regimens. Urokinase-type plasminogen activator (u-PA) and matrix metalloproteinases (MMP) have been implicated in cardiac inflammation, matrix remodeling, and wound healing after cardiac injury. The present review will assess the mechanism by which these proteinases mediate cardiac dilatation, fibrosis, and dysfunction after cardiac stress or injury, in order to understand how inhibition of proteinases may provide a novel therapeutic tool to prevent cardiac dilatation and failure during viral myocarditis. [ABSTRACT FROM AUTHOR]

Published
2006
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146. Prognostic Relevance of Gene-Environment Interactions in Patients With Dilated Cardiomyopathy Applying the MOGE(S) Classification

Author

Hazebroek, M.R., Moors, S., Dennert, R., van den Wijngaard, A., Krapels, I., Hoos, M., Verdonschot, J., Merken, J.J., de Vries, B., Wolffs, P.F., Crijns, H.J.G.M., Brunner-La Rocca, H.P., Heymans, S., Klinische Genetica, Kindergeneeskunde, Algemene Heelkunde, Med Microbiol, Infect Dis & Infect Prev, Cardiologie, RS: CAPHRI School for Public Health and Primary Care, RS: CARIM - R2 - Cardiac function and failure, RS: CAPHRI - R4 - Health Inequities and Societal Participation, Genetica & Celbiologie, and Pathologie

Subjects
MUTATIONS, etiology, autoimmune, virus, toxic, CARDIOLOGY WORKING GROUP, DIAGNOSIS, EUROPEAN-SOCIETY, DYSFUNCTION, PERICARDIAL DISEASES, HEART-FAILURE, POSITION STATEMENT, MYOCARDIUM, TASK-FORCE
Abstract

BACKGROUND The multifactorial pathogenesis leading to dilated cardiomyopathy (DCM) makes stratification difficult. The recent MOGE(S) (morphofunctional, organ involvement, genetic or familial, etiology, stage) classification addresses this issue. OBJECTIVES The purpose of this study was to investigate the applicability and prognostic relevance of the MOGE(S) classification in patients with DCM. METHODS This study used patients from the Maastricht Cardiomyopathy Registry in the Netherlands and excluded patients with ischemic, valvular, hypertensive, and congenital heart disease. All other patients underwent a complete diagnostic work-up, including genetic evaluation and endomyocardial biopsy. RESULTS A total of 213 consecutive patients with DCM were included: organ involvement was demonstrated in 35 (16%) and genetic or familial DCM in 70 (33%) patients, including 16 (8%) patients with a pathogenic mutation. At least 1 cause was found in 155 (73%) patients, of whom 48 (23%) had more than 1 possible cause. Left ventricular reverse remodeling was more common in patients with nongenetic or nonfamilial DCM than in patients with genetic or familial DCM (40% vs. 25%; p = 0.04). After a median follow-up of 47 months, organ involvement and higher New York Heart Association functional class were associated with adverse outcome (p = 2 vs. CONCLUSIONS The MOGE(S) classification in DCM is applicable, and each attribute or the gene-environment interaction is associated with outcome. Importantly, the presence of multiple attributes was a strong predictor of adverse outcome. Finally, adaptation of the MOGE(S) involving multiple possible etiologies is recommended. (C) 2015 by the American College of Cardiology Foundation.

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149. Renal function estimation and Cockroft-Gault formulas for predicting cardiovascular mortality in population-based, cardiovascular risk, heart failure and post-myocardial infarction cohorts: The Heart 'OMics' in AGEing (HOMAGE) and the high-risk myocardial infarction database initiatives

Author

João Pedro Ferreira, Girerd N, Pellicori P, Duarte K, Girerd S, Ma, Pfeffer, Jj, Mcmurray, Pitt B, Dickstein K, Jacobs L, Ja, Staessen, Butler J, Latini R, Masson S, Mebazaa A, Hp, Rocca, Delles C, Heymans S, Sattar N, and Jw, Jukema

150. The FLNC gene in myopathies and cardiomyopathies

Author

Vanhoutte, E., Verdonschot, J., Claes, G., Helderman-Van Den Enden, A., Hoeijmakers, J., Hellebrekers, D., Haan, A., Christiaans, I., Lekanne-Deprez, R., Craenenbroeck, E., Boen, H., Loeys, B., Hoedemakers, Y., Carlo Marcelis, Kempers, M., Brusse, E., Waning, J., Baas, A., Dooijes, D., Asselbergs, F., Barge-Schaapveld, D., Koopman, P., Den Wijngaard, A., Heymans, S., Krapels, I., and Brunner, H.

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