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Single-cell sequencing quantitative analysis of skin tissues of wild-type and Chrna5-/- mice treated with imiquimod

ABSTRACT: Purpose: To understand the molecular processes and cell subsets involved in an increase in the psoriatic inflammatory response in Chrna5 signaling compared with WT mice, we performed single-cell sequencing with dorsal skin tissues after IMQ and vaseline treatment. Methods: Skin mRNA profiles of wile-type (WT) and cholinergic receptor nicotinic alpha 5 subunit knockout (Chrna5-/-)mice were generated by deep sequencing. The samples of KO and WT mice after IMQ and vaseline treatment were processed in terms of alignment, barcode assignment, and UMI counting with Cell Ranger, version 3.0.2 (https://github.com/10XGenomics/cellranger) count pipeline. Results: The cell clustering analysis , the heat map analysis , the cell subpopulations of keratinocytes analysis, the gene enrichment analysis and signal pathway analysis were all carried out . The results of these studies indicated that Chrna5 knockout has a significant effect on the proliferation of keratinocytes after IMQ treatment. Further gene analysis and signal pathway analysis showed that Chrna5 knockout down-regulated the JAK/STAT signal pathway, which is a key signal pathway for the occurrence and development of psoriasis. Conclusions: These results revealed the potential role of Chrna5 in the occurrence and development of psoriasis, and provided a basis for it as a potential drug target.

ORGANISM(S): Mus musculus

PROVIDER: GSE193350 | GEO | 2022/02/28

REPOSITORIES: GEO

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Project description:Background: Imiquimod (IMQ) produces a cutaneous phenotype in mice frequently studied as an acute model of human psoriasis. Whether this phenotype depends on strain or sex has never been systematically investigated on a large scale. Such effects, however, could lead to conflicts among studies, while further impacting study outcomes and efforts to translate research findings. Methods: RNA-seq was used to evaluate the psoriasiform phenotype elicited by IMQ in both sexes of 7 mouse strains (C57BL/6J, BALB/cJ, CD1, DBA/1J, FVB/NJ, 129X1/SvJ and MOLF/EiJ). Results: In most strains, IMQ altered gene expression in a manner consistent with human psoriasis, partly due to innate immune activation and decreased homeostatic gene expression. The IMQ response of MOLF males was aberrant, however, with decreased expression of differentiation-associated genes (elevated in other strains). Key aspects of the IMQ response differed between the two most commonly studied strains (BALB/c and C57BL/6). Compared with BALB/c, the C57BL/6 phenotype showed increased expression of genes associated with DNA replication, IL-17A activation and CD8+ T cells, but decreased expression of genes associated with interferon signaling and CD4+ T cells. Surprisingly, although IMQ-induced expression shifts mirrored psoriasis, correspondence was similar or better for other human skin diseases (e.g., eschars, acne, atopic dermatitis). For BALB/c, MOLF, and 129X1 strains, genes altered by IMQ corresponded better to those altered in human skin infections or wounds compared with those altered in psoriasis lesions. Conclusions: These findings demonstrate strain-dependent aspects of IMQ dermatitis that warrant consideration in planning and interpreting experimental studies. We have further shown that IMQ does not uniquely model psoriasis but in fact triggers a core set of pathways active in diverse skin diseases. These observations challenge the view of IMQ dermatitis as a mouse phenotype uniquely appropriate for studying psoriasis as opposed to other human skin conditions.

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Single-cell sequencing quantitative analysis of skin tissues of wild-type and Chrna5-/- mice treated with imiquimod

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