1453 LncRNA SNHG26 facilitates inflammatory to proliferative state transition of keratinocyte progenitors during wound healing

The cell transition from an inflammatory phase to a subsequent proliferative is crucial for wound healing; however, the mechanism driving this not well understood. By profiling lncRNA expression changes during human skin healing and screening functions, we identified SNHG26, conserved upregulated healing, as pivotal regulator in keratinocyte progenitor cells underpinning transition.Snhg26-deficient mice exhibited impaired repair characterized by delayed re-epithelization accompanied exacerbated inflammation. A single-cell transcriptome analysis revealed that number of basal keratinocytes or migratory state was decreased, whereas were increased wound-edges Snhg26-deficient mice. Furthermore, validated promigratory anti-inflammatory functions SNHG26 progenitors. Importantly, inhibition severely re-epithelialization ex vivo wounds. mechanistic study interacted with relocated transcription factor ILF2 genomic loci, such JUN, IL6, IL8, CCL20, locus LAMB3, rewiring gene program facilitate inflammatory-to-proliferative Collectively, our findings suggest lncRNAs play cardinal roles expediting tissue regeneration may constitute invaluable reservoir therapeutic targets reparative medicine.