Non-muscle myosin II regulates survival threshold of pluripotent stem cells

Andrea Walker, Hua Su, Mary Anne Conti, Nicole Harb, Robert S. Adelstein and Noboru Sato ()
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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

Nature Communications, 2010, vol. 1, issue 1, 1-9

Abstract: 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.

Date: 2010
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DOI: 10.1038/ncomms1074

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