AKAP121 downregulation impairs protective cAMP signals, promotes mitochondrial dysfunction, and increases oxidative stress

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Abstract

Competitive peptides displacing AKAP121 from mitochondria in the tissue and in the cells were used to investigate the role of AKAP121 in mitochondrial function, reactive oxygen species (ROS) generation, and cell survival. Displacement of AKAP121 from mitochondria by synthetic peptides triggers the death program in cardiomyocytes. Under pathological conditions in vivo, in a rat model of cardiac hypertrophy induced by ascending aorta banding, the levels of AKAP121 are significantly down-regulated. Disappearance of AKAP121 is associated with mitochondrial dysfunction, high oxidative stress, and apoptosis. In vivo delocalization of AKAP121 by competitive peptides replicates some of the molecular signatures induced by pressure overload: mitochondrial dysfunction, increased mitochondrial ROS, and apoptosis.

Autore Pugliese

Tutti gli autori

  • Perrino C.; Feliciello A.; Schiattarella G.G.; Esposito G.; Guerriero R.; Zaccaro L.; Del Gatto A.; Saviano M.; Garbi C.; Carangi R.; Di Lorenzo E.; Donato G.; Indolfi C.; Avvedimento V.E.; Chiariello M.

Titolo volume/Rivista

Cardiovascular research

Anno di pubblicazione

2010

ISSN

0008-6363

ISBN

Non Disponibile

Numero di citazioni Wos

Nessuna citazione

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Numero di citazioni Scopus

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Ultimo Aggiornamento Citazioni

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Settori ERC

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Codici ASJC

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