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

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

PROVIDER: PRJNA903815 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22356561_1.fastq.gz	Fastqsanger.gz
	SRR22356561_2.fastq.gz	Fastqsanger.gz
	SRR22356562_1.fastq.gz	Fastqsanger.gz
	SRR22356562_2.fastq.gz	Fastqsanger.gz
	SRR22356563_1.fastq.gz	Fastqsanger.gz

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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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Project description:The wounds were made on the back skin of Snhg26 knockout (KO) and wild type (WT) mice. The wound edge and skin tissue were collected and the epidermis were separated by incubate the tissue with dispaseII. Total RNA was extracted from the epidermis. The global transcriptome analysis of the epidermis were performed by using Affymetrix arrays.

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Project description:Olfactomedin-4 (OLFM4) is an olfactomedin-domain-containing glycoprotein which regulates cell adhesion, proliferation, gastrointestinal inflammation, innate immunity and cancer metastasis. In the present study investigated its role in skin regeneration and wound healing. We found that OLFM4 expression is transiently upregulated in the proliferative phase of cutaneous wound healing in humans as well as in mice. Moreover, a significant increase in OLFM4 expression was detected in the skin of lesional psoriasis, a chronic inflammatory disease characterized by keratinocyte hyperproliferation. In vitro experiments demonstrated that OLFM4 can selectively stimulate keratinocyte proliferation and increase both keratinocyte and fibroblast migration ability. Using proteotransciptomic pathway analysis we revealed that transcription factors POU5F1/OCT4 and ESR1 acted as hubs for OLFM4-dependent signalling in keratinocytes. In vivo experiments utilizing mouse splinted full-thickness cutaneous wound healing model showed that application of recombinant OLFM4 protein can significantly improve wound healing time. Taken together, our results suggest that OLFM4 is a transiently upregulated inflammatory signal that promotes wound healing by supporting the functions of both dermal and epidermal cell compartments.

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