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Assessing the cellular microenvironment in the skin of mice lacking epidermal Pparg compared with wildtype sibling controls.

ABSTRACT: B6.129-Ppargtm2Rev/J mice (Stock Number: 004584, The Jackson Laboratory) were crossed with B6N.Cg-Tg(KRT14-cre)1Amc/J mice (Stock Number 018964, The Jackson Laboratory) to generate epidermal-specific PPARγ knockout mice in the C57BL/6J background (C57.Pparg-/-epi mice). Mice were housed under specific pathogen-free conditions at the Indiana University School of Medicine. The protocols were approved by the Indiana University School of Medicine Institutional Animal Care and Use Committee (IACUC). Using whole transcriptomic RNA sequencing (GSE164024), we had previously demonstrated that the skin of mice lacking epidermal Pparg exhibited signficant changes in approximately 12% of the expressed genes, formed spontaneous inflammatory skin lesions, and had prominent increases in pro-inflammatory genes and a reduction in genes associated with the epidermal lipid barrier function. Mice lacking epidermal Pparg are also prone to increase chemical and photocarcinogenesis. We therefore sought to determine the changes in gene expression at the cellular level to obtain information regarding changes to the cellular microenvironment within the skin of Pparg-/-epi mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE320138 | GEO | 2026/02/24

REPOSITORIES: GEO

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Project description:Both agonist studies and loss-of-function models indicate that PPARγ plays an important role in cutaneous biology. Since PPARγ has a high level of basal activity, we hypothesized that epidermal PPARγ would regulate normal homeostatic processes within the epidermis. In this current study, we performed mRNA sequencing and differential expression analysis of epidermal scrapings from knockout mice and wildtype littermates. Pparg-/-epi mice exhibited a 1.5-fold or greater change in the expression of 11.8% of 14,482 identified transcripts. Up-regulated transcripts included those for a large number of cytokines/chemokines and their receptors, as well as genes associated with inflammasome activation and keratinization. Several of the most dramatically up-regulated pro-inflammatory genes in Pparg-/-epi mouse skin included Igfl3, 2610528A11Rik, & Il1f6. RT-PCR was performed from RNA obtained from non-lesional full-thickness skin and verified a marked increase in these transcripts, as well as transcripts for Igflr1, which encodes the receptor for Igfl3, and the 2610528A11Rik receptor (Gpr15). Transcripts for Il4 were detected in Pparg-/-epi mouse skin, but transcripts for Il17 & Il22 were not detected. Down-regulated transcripts included sebaceous gland markers and a number of genes associated with lipid barrier formation. The change in these transcripts correlates with an asebia phenotype, increased transepidermal water loss, alopecia, dandruff and the appearance of spontaneous inflammatory skin lesions. Histologically, non-lesional skin showed hyperkeratosis, while inflammatory lesions were characterized by dermal inflammation and epidermal acanthosis, spongiosis, and parakeratosis. In conclusion, loss of epidermal Pparg alters a substantial set of genes that are associated with cutaneous inflammation, keratinization and sebaceous gland function. This data indicates that epidermal PPARγ plays an important role in homeostatic epidermal function, particularly epidermal differentiation, barrier function, sebaceous gland development and function, and inflammatory signaling.

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Assessing the cellular microenvironment in the skin of mice lacking epidermal Pparg compared with wildtype sibling controls.

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