PUMA is critical for neonatal cardiomyocyte apoptosis induced by endoplasmic reticulum stress.

ABSTRACT:

Objective

Puma (p53-upregulated modulator of apoptosis), a proapoptotic BH3-only member of the Bcl-2 protein family, has been implicated in the pathomechanism of several diseases, including cancer, AIDS, and ischemic brain disease. We have recently shown that Puma is required for cardiac cell death upon ischemia/reperfusion of mouse hearts. Since ischemia/reperfusion is also associated with endoplasmic reticulum (ER) stress, in the present study we investigated whether Puma contributes to the ER stress-dependent component of cardiomyocyte apoptosis.

Methods

Primary cultures of rat and mouse neonatal cardiomyocytes were treated with 3 muM thapsigargin or 100 ng mL(-1) tunicamycin. Puma levels were suppressed by adenoviral delivery of shRNA or targeted deletion of the puma gen

SUBMITTER: Nickson P 

PROVIDER: S-EPMC1832123 | biostudies-literature | 2007 Jan

REPOSITORIES: biostudies-literature