 
- 积分
- 306
- 威望
- 306
- 包包
- 3648
|

Nature Communications 1 , Article number: 71 doi:10.1038/ncomms1074 * v4 s/ g" [! p- W8 L
+ I- W- f, w) s
Non-muscle myosin II regulates survival threshold of pluripotent stem cells
: }) \; d& B7 M/ v& ?" G5 N
4 ]) e9 L4 d9 c: a3 zAndrea Walker, Hua Su,Mary Anne Conti,Nicole Harb,Robert S. Adelstein& Noboru Sato
: r# h6 l+ G) Y, d1 z2 O( D6 Q1 k
# [8 b" N" R, m/ s) JHuman 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 |
|