PATCH

Targeting the miR-106b~25 cluster in pathological Cardiac Hypertrophy

Coordinatore	INTERNATIONAL CENTRE FOR GENETIC ENGINEERING AND BIOTECHNOLOGY    more  Organization address address: PADRICIANO 99 city: TRIESTE postcode: 34149 contact info Titolo: Mr. Nome: Decio Cognome: Ripandelli Email: send email Telefono: +39 040 3757345 Fax: +39 040 3757363
Nazionalità Coordinatore	Italy [IT]
Totale costo	93˙707 €
EC contributo	93˙707 €
Programma	FP7-PEOPLE Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	FP7-PEOPLE-2013-IEF
Funding Scheme	MC-IEF
Anno di inizio	2014
Periodo (anno-mese-giorno)	2014-03-01   -   2015-02-28

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	INTERNATIONAL CENTRE FOR GENETIC ENGINEERING AND BIOTECHNOLOGY  Organization address address: PADRICIANO 99 city: TRIESTE postcode: 34149 contact info Titolo: Mr. Nome: Decio Cognome: Ripandelli Email: send email Telefono: +39 040 3757345 Fax: +39 040 3757363	IT (TRIESTE)	coordinator	93˙707.40

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 Obiettivo del progetto (Objective)

'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.'