Abstract：
:Diminished mitochondrial function is causally related to some heart diseases. Here, we developed a human disease model based on cardiomyocytes from human embryonic stem cells (hESCs), in which an important pathway of mitochondrial gene expression was inactivated. Repression of PGC-1α, which is normally induced during development of cardiomyocytes, decreased mitochondrial content and activity and decreased the capacity for coping with energetic stress. Yet, concurrently, reactive oxygen species (ROS) levels were lowered, and the amplitude of the action potential and the maximum amplitude of the calcium transient were in fact increased. Importantly, in control cardiomyocytes, lowering ROS levels emulated this beneficial effect of PGC-1α knockdown and similarly increased the calcium transient amplitude. Our results suggest that controlling ROS levels may be of key physiological importance for recapitulating mature cardiomyocyte phenotypes, and the combination of bioassays used in this study may have broad application in the analysis of cardiac physiology pertaining to disease.
journal_name
Stem Cell Reportsjournal_title
Stem cell reportsauthors
Birket MJ,Casini S,Kosmidis G,Elliott DA,Gerencser AA,Baartscheer A,Schumacher C,Mastroberardino PG,Elefanty AG,Stanley EG,Mummery CLdoi
10.1016/j.stemcr.2013.11.008subject
Has Abstractpub_date
2013-12-12 00:00:00pages
560-74issue
6issn
2213-6711pii
S2213-6711(13)00148-3journal_volume
1pub_type
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