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Epigenetic Switch Reshapes Epithelial Stem/Progenitor Cells Signatures and Contributes to Inflammatory Programming in Hidradenitis Suppurativa [ATAC-seq]

ABSTRACT: Epigenetic Switch Reshapes Epithelial Stem/Progenitor Cells Signatures and Contributes to Inflammatory Programming in Hidradenitis Suppurativa [ATAC-seq]

PROVIDER: PRJNA940165 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23681784_1.fastq.gz	Fastqsanger.gz
	SRR23681784_2.fastq.gz	Fastqsanger.gz
	SRR23681785_1.fastq.gz	Fastqsanger.gz
	SRR23681785_2.fastq.gz	Fastqsanger.gz
	SRR23681786_1.fastq.gz	Fastqsanger.gz

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Epigenetic Switch Reshapes Epithelial Stem/Progenitor Cells Signatures and Contributes to Inflammatory Programming in Hidradenitis Suppurativa

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Epigenetic Switch Reshapes Epithelial Stem/Progenitor Cells Signatures and Contributes to Inflammatory Programming in Hidradenitis Suppurativa [CUT&RUN]

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Epigenetic Switch Reshapes Epithelial Stem/Progenitor Cells Signatures and Contributes to Inflammatory Programming in Hidradenitis Suppurativa [RNA-seq]

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Gene expression profiling of blood in hidradenitis suppurativa

Project description:To acquire a better understanding of the molecular pathogenesis of hidradenitis suppurativa (HS), we performed mRNA microarray studies to compare whole blood gene expression of HS patients to that of healthy normal subjects. No significant difference was observed in whole blood mRNA expression between HS patients and healthy normal control. Whole blood samples were collected from patients with hidradenitis (n=16) at baseline and healthy normal subjects (n=10) for RNA extraction and microarray analysis.

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Epigenetic Switch Reshapes Epithelial Stem/Progenitor Cells Signatures and Contributes to Inflammatory Programming in Hidradenitis Suppurativa [scRNA-seq]

Project description:In this study, we used single-cell RNA-sequencing to reveal how cellular heterogeneity of Hidradenitis Suppurativa (HS) lesional epidermis was reshaped at the transcriptional level. By comparison with healthy interfollicular epidermal basal cells, in HS we revealed marked gene signatures centered on mitotic chromosome segregation, DNA replication and repair as well as cell-cell adhesion and chromatic remodeling. Combing the pseudotime-ordered single-cell trajectory with the spatial localization analysis of defined basal cells, we further identified and validated a global alteration in cellular diversity within HS epidermis characterized by basal I-III cells hyperproliferation, concomitant decreases in superbasal keratinocytes, and phenotypic shifts toward the S100A cluster highly expressing pro-inflammatory genes S100A7/8/9. Cell-cell communication modeling suggested that HS BIII keratinocytes and S100A population serve as a crucial source to trigger IL-1 and IL-10 inflammatory cascades in the disease progression.

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Project description:Hidradenitis suppurativa (HS), also termed acne inversa, is a persistent inflammatory dermatological condition affecting approximately 1% of the global population, causing significant morbidity. The etiology of HS is not fully elucidated, but it is known that immune dysfunction plays a critical role. In our research to discern the role of non-coding RNA in HS, we initially conducted a comparative analysis of the most significantly altered long non-coding RNA (lncRNA) and mRNA expressions.

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