Expression data from Werner syndrome iPSCs. Homo sapiens

Werner syndrome (WS) is a premature aging disorder characterized by chromosomal instability and cancer predisposition. Mutations in WRN are responsible for the disease and cause telomere dysfunction, resulting in accelerated aging. In the present study, we describe the effects of long-term culture on WS iPSCs, which acquired and maintained infinite proliferative potential for self-renewal over 2 years. After long-term cultures, WS iPSCs exhibited stable undifferentiated states and differentiation capacity, and premature upregulation of senescence-associated genes in WS cells was completely suppressed in WS iPSCs despite WRN deficiency. We used microarrays to examine whether global gene expression profile of WS iPSCs is similar to that of normal iPSCs and human ESCs, as well as premature senescence phenotype is suppressed by reprogramming. Overall design: Total RNAs extracted from WS fibroblasts, WS iPSCs, normal iPSCs, and human ESCs were hybridized onto Human Genome U133 Plus 2.0 Arrays to compare global gene expression profile of WS iPSCs with normal human pluripotent stem cells, as well as the parental fibroblasts.