In Nature this week, researchers from the University of Sheffield report on a novel cell-based treatment for auditory neuropathy, a form of deafness characterized by damage to spiral ganglion neurons with relative preservation of sensory hair cells. Using human embryonic stem cells, the team generated ear-cell progenitors capable of differentiating into hair cells and auditory neurons. When introduced into a gerbil model of auditory neuropathy, the cells were able to restore auditory responses in the brainstem.
Also this week, investigators from the Howard Hughes Medical Institute and collaborators published data establishing increased proteasome activity as an "intrinsic characteristic" of human embryonic stem cell identity. Noting that genomic stability is vital for stem cell survival, the team suggests that proteome stability may have an equally important role, in part because of the potential for passage of damaged proteins to daughter cells through asymmetric division. They found that human embryonic stem cells show high proteasome activity correlated with increased levels of the 19S proteasome subunit PSMD11 and a corresponding increase in assembly of the 26S/30S proteasome. Additionally, proteasome inhibition in the stem cells affects the expression of pluripotency markers and the levels of specific markers of the distinct germ layers. The findings suggest a "new regulation of proteostasis" in human embryonic stem cells that links longevity and stress resistance in invertebrates to the cells' function and identity.
Meanwhile, in Nature Genetics, Oxford University scientists report on the identification of genetic variants associated with Barrett's esophagus, a premalignant condition linked to damage to the esophageal lining from acid reflux. The team conducted the first genome-wide association study on the condition, comprising 1,852 cases and 5,172 controls in the UK in the discovery stage, and 5,986 cases and 12,825 controls in the replication stage. They found that variants at two loci were associated with disease risk as well as evidence that "many common variants of small effect contribute to genetic susceptibility to Barrett's esophagus and that [single-nucleotide polymorphism] alleles predisposing to obesity also increase risk for Barrett's esophagus."