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Keratinocyte response to SNHG26 silencing

ABSTRACT: Keratinocyte response to SNHG26 silencing

PROVIDER: PRJNA895451 | ENA |

REPOSITORIES: ENA

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Keratinocyte response to SNHG26 silencing

Project description:Analysis the transcriptome of keratinocyte after SNHG26 silencing with or without TNFa treatment for 3 hours. SNHG26 is a conseved lncRNA which is upregulated in the epidermis of human and mouse acute wound. Results of this profiling provide insight into the biological role of SNHG26 in keratinocytes.

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

Project description:The epidermal stem cell transition from inflammation to proliferation is a crucial process in tissue repair. However, the molecular mechanism underlying this process is poorly understood. Combined with lncRNA expression profiling of human acute wounds and functional screening, we identified SNHG26 as a pivotal regulator of inflammatory to proliferative state transition of keratinocyte progenitor cells. Snhg26-deficient mice showed impaired wound healing characterized by increased inflammatory response and decreased reepithelization in the wound. Consistently, single-cell transcriptomic analysis of the wound-edge tissue identified proliferative, migratory, and proinflammatory basal progenitors, which were dramatically changed in Snhg26 deficient mice. Mechanically, SNHG26 binds with ILF2 to relocate this transcription factor from the inflammatory gene loci (such as JUN) to the LAMB3 genomic loci. Collectively, this work identified a conserved lncRNA SNHG26 as a master regulator of epidermal stem cell state transition from inflammation to proliferation, highlighting the importance of lncRNAs in tissue repair and regeneration.

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