PATCH

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

 Coordinatore 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

 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

Mappa


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cluster    generation    therapeutic    pathological    heart    cardiac    mice    hypertrophy    mir    therapies       virus    data    transcriptional    remodeling    direct    mirs    downstream   

 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.'

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