Author: ["John A Muraski","Marcello Rota","Yu Misao","Jenna Fransioli","Christopher Cottage","Natalie Gude","Grazia Esposito","Francesca Delucchi","Michael Arcarese","Roberto Alvarez","Sailay Siddiqi","Gregory N Emmanuel","Weitao Wu","Kimberlee Fischer","Joshua J Martindale","Christopher C Glembotski","Annarosa Leri","Jan Kajstura","Nancy Magnuson","Anton Berns","Remus M Beretta","Steven R Houser","Erik M Schaefer","Piero Anversa","Mark A Sussman"]
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Abstract
The serine-threonine kinases Pim-1 and Akt regulate cellular proliferation and survival. Although Akt is known to be a crucial signaling protein in the myocardium, the role of Pim-1 has been overlooked. Pim-1 expression in the myocardium of mice decreased during postnatal development, re-emerged after acute pathological injury in mice and was increased in failing hearts of both mice and humans. Cardioprotective stimuli associated with Akt activation induced Pim-1 expression, but compensatory increases in Akt abundance and phosphorylation after pathological injury by infarction or pressure overload did not protect the myocardium in Pim-1–deficient mice. Transgenic expression of Pim-1 in the myocardium protected mice from infarction injury, and Pim-1 expression inhibited cardiomyocyte apoptosis with concomitant increases in Bcl-2 and Bcl-XL protein levels, as well as in Bad phosphorylation levels. Relative to nontransgenic controls, calcium dynamics were significantly enhanced in Pim-1–overexpressing transgenic hearts, associated with increased expression of SERCA2a, and were depressed in Pim-1–deficient hearts. Collectively, these data suggest that Pim-1 is a crucial facet of cardioprotection downstream of Akt.Cite this article
Muraski, J., Rota, M., Misao, Y. et al. Pim-1 regulates cardiomyocyte survival downstream of Akt. Nat Med 13, 1467–1475 (2007). https://doi.org/10.1038/nm1671 