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. 2005 Oct;14(5):593-604.
doi: 10.1007/s11248-005-4350-5.

Partial correction of abnormal cardiac development in caspase-8-deficient mice by cardiomyocyte expression of p 35

Nobuyuki Yajima  1 , Shu-Ichi Yamada, Takayuki Morisaki, Shinya Toyokuni, Shin Yonehara, Kazuhiro Sakamaki
Affiliations

Partial correction of abnormal cardiac development in caspase-8-deficient mice by cardiomyocyte expression of p 35

Nobuyuki Yajima et al. Transgenic Res. 2005 Oct.

Abstract

Baculovirus p 35 protein protects cells from apoptotic cell death by inhibiting caspase activation. We have established transgenic mouse lines specifically expressing p 35 in cardiomyocytes, and primary cardiomyocytes isolated from these mice exhibit resistance to staurosporine-induced apoptosis. In a previous study, we observed defects in heart formation associated with abdominal hemorrhage and cardiomyocyte cell death in caspase-8-deficient animals. In order to better understand the etiology of the cardiac defects and embryonic lethality in caspase-8-deficient mice, we crossed these mice with the p 35 transgenic animals. Although the newly generated mice still died in utero and exhibited some cardiac defects, cardiomyocyte apoptosis was suppressed and ventricular trabeculation was restored. Thus, cardiomyocyte expression of p 35 prevented cell death induced by staurosporine or caspase-8 deficiency. Additionally, our data suggest that caspase-8 plays multiple roles in cardiac development.

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