Author
Listed:
- Andrea Walker
(University of California, Riverside)
- Hua Su
(University of California, Riverside)
- Mary Anne Conti
(Laboratory of Molecular Cardiology, National Heart, Lung, and Blood Institute, National Institutes of Health)
- Nicole Harb
(University of California, Riverside)
- Robert S. Adelstein
(Laboratory of Molecular Cardiology, National Heart, Lung, and Blood Institute, National Institutes of Health)
- Noboru Sato
(University of California, Riverside)
Abstract
Human pluripotent stem (hPS) cells such as human embryonic stem (hES) and induced pluripotent stem (hiPS) cells are vulnerable under single cell conditions, which hampers practical applications; yet, the mechanisms underlying this cell death remain elusive. In this paper, we demonstrate that treatment with a specific inhibitor of non-muscle myosin II (NMII), blebbistatin, enhances the survival of hPS cells under clonal density and suspension conditions, and, in combination with a synthetic matrix, supports a fully defined environment for self-renewal. Consistent with this, genetically engineered mouse embryonic stem cells lacking an isoform of NMII heavy chain (NMHCII), or hES cells expressing a short hairpin RNA to knock down NMHCII, show greater viability than controls. Moreover, NMII inhibition increases the expression of self-renewal regulators Oct3/4 and Nanog, suggesting a mechanistic connection between NMII and self-renewal. These results underscore the importance of the molecular motor, NMII, as a novel target for chemically engineering the survival and self-renewal of hPS cells.
Suggested Citation
Andrea Walker & Hua Su & Mary Anne Conti & Nicole Harb & Robert S. Adelstein & Noboru Sato, 2010.
"Non-muscle myosin II regulates survival threshold of pluripotent stem cells,"
Nature Communications, Nature, vol. 1(1), pages 1-9, December.
Handle:
RePEc:nat:natcom:v:1:y:2010:i:1:d:10.1038_ncomms1074
DOI: 10.1038/ncomms1074
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