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Targeting the miR 106b 25 cluster in pathological Cardiac Hypertrophy

BACKGROUND: There is a tremendous need to develop novel therapies for heart failure. In particular, sustained pathological hypertrophy, a major predictor of this condition, is a complex process, which involves transcriptional and... ver más

28/02/2015

INCE

94K€

Presupuesto del proyecto: 94K€

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INCE INIZIATIVA CENTRO EUROPEA - SEGRETARIATO... No se ha especificado una descripción o un objeto social para esta compañía.

Fecha límite participación Sin fecha límite de participación.

Financiación concedida El organismo FP7 notifico la concesión del proyecto el día 2015-02-28 No tenemos la información de la convocatoria

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Líder del proyecto

INCE INIZIATIVA CENTRO EUROPEA - SEGRETARIATO... No se ha especificado una descripción o un objeto social para esta compañía.

Presupuesto del proyecto 94K€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto BACKGROUND: There is a tremendous need to develop novel therapies for heart failure. In particular, sustained pathological hypertrophy, a major predictor of this condition, is a complex process, which involves transcriptional and posttranscriptional regulation of the cardiac genome. There is now clear indication that, besides a few known transcriptional regulators, multiple, still poorly understood cardiac factors are involved in hypertrophy; understanding this complexity is expected to pave to the way to innovative therapies. In particular, recent data demonstrate that dysregulated microRNAs (miRs) are associated with heart failure, and that selective modulation of miRs can provide therapeutic benefits. Our pilot-data show that expression of the miR-106b~25 cluster decreases during pathological hypertrophy in mice and that virus-mediated overexpression of this cluster prevents phenylephrine-induced hypertrophic remodeling. Following bioinformatics screens for potential direct downstream targets of the miR-25~106b cluster, we identified a series of transcription factors, which might play a role in pathological cardiac remodeling. AIM: To define the functional implication of the miR-106b~25 cluster in pathological cardiac hypertrophy and to exploit this information towards the development of novel therapeutic approaches. APPROACH: We will identify direct downstream targets of the miR-106b~25 cluster during hypertrophy, by performing Ago2-Immunoprecipitation and by treating neonatal cardiomyocytes with precursors of miR-25, miR-93 and miR-106b, followed by next generation sequencing (Objective 1); We aim to reverse pathological cardiac remodeling and prevent heart failure by delivery of recombinant adeno-associated virus (rAAV9)- miR-106b~25 in mice (Objective 2). The results obtained will generate important intellectual property value and will constitute the basis for further development towards the generation of novel therapies against heart failure.

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