Mitochondria in human pluripotent stem cell apoptosis. (April 2016)

• Record Type: Journal Article
• Authors: TeSlaa, Tara; Setoguchi, Kiyoko; Teitell, Michael A.
• Is Part Of: Seminars in cell & developmental biology. Volume 52(2016)
• Page Start: 76
• Page End: 83
• Publication Date: 2016-04
• Subjects: BAK BCL-2 antagonist killer -- BAX BCL-2 associated X protein -- CDK1 cyclin dependent kinase 1 -- CLDN-6 claudin-6 -- CM cardiomyocyte -- CPE Clostridium perfringens endotoxin -- GPX2 glutathione peroxidase-2 -- GSH glutathione -- GSR glutathione reductase -- GSSG glutathione disulfide -- hESC human embryonic stem cell -- hiPSC human induced pluripotent stem cell -- hPSC human pluripotent stem cell -- IMS intermembrane space -- MDM2 mouse double minute 2 homolog -- MMR mismatch repair -- MOMP mitochondrial outer membrane permeabilization -- NAMPT nicotinamide phosphoribosyltransferase -- OXPHOS oxidative phosphorylation -- PPP pentose phosphate pathway -- ROCK Rho-associated kinase -- ROS reactive oxygen species -- SCD1 stearoyl-coA desaturase -- UCP2 uncoupling protein 2; Apoptosis -- Human pluripotent stem cells -- p53 -- Tumorigenicity; Cytology -- Periodicals; Developmental biology -- Periodicals; 571.6
• DOI: 10.1016/j.semcdb.2016.01.027
• Languages: English
• ISSNs: 1084-9521

Abstract

Abstract: Human pluripotent stem cells (hPSCs) have great potential in regenerative medicine because they can differentiate into any cell type in the body. Genome integrity is vital for human development and for high fidelity passage of genetic information across generations through the germ line. To ensure genome stability, hPSCs maintain a lower rate of mutation than somatic cells and undergo rapid apoptosis in response to DNA damage and additional cell stresses. Furthermore, cellular metabolism and the cell cycle are also differentially regulated between cells in pluripotent and differentiated states and can aid in protecting hPSCs against DNA damage and damaged cell propagation. Despite these safeguards, clinical use of hPSC derivatives could be compromised by tumorigenic potential and possible malignant transformation from failed to differentiate cells. Since hPSCs and mature cells differentially respond to cell stress, it may be possible to specifically target undifferentiated cells for rapid apoptosis in mixed cell populations to enable safer use of hPSC-differentiated cells in patients.