Project description:Study to optimize our protocol for isolating RNA from skin biopsies from (hairless) SKH mice using different-diameter biopsy punches. Some mice were also treated with UVB radiation to check its effect on RNA yield.
Project description:To investigate the effecs of commensal papillomavirus immunity on the homeostasis of highly mutated normal skin, spatial transcriptomics (Xenium, 10x Genomics, Pleasanton, CA) was performed on SKH-1 mouse back skin. The mice were treated with mouse papillomavirus (MmuPV1) or virus-like particles (VLP), followed by UV exposure for 25 weeks.
Project description:Study to optimize our protocol for isolating RNA from skin biopsies from (hairless) SKH mice using different-diameter biopsy punches. Some mice were also treated with UVB radiation to check its effect on RNA yield. 4 mice total: 2 were irradiated with 300J/m2 UVB and 2 were non-irradiated. Post-mortem skin biopsies with 1.5mm, 2.0mm, and 2.5mm diameter punches were taken from the dorsal region.
Project description:The immune checkpoint ligand PD-L1 has emerged as a molecular target for skin cancer therapy and might also hold promise for preventive intervention targeting solar ultraviolet light-induced skin damage. Topical application of the small molecule PD-L1 inhibitor BMS-202 significantly modulates UV-induced inflammation in SKH-1 mouse skin as substantiated by NanoString CounterTM transcriptomic analysis.
Project description:We used RNA-Seq to search for potential downstream effectors of GNAQ R183Q during the developent of vascular phenotypes in the mouse back skin.
Project description:Mice are cancer-prone, whereas naked mole-rats are cancer-resistant. To test the discrepancies between how mouse and naked mole-rat skin responds to carcinogens, we topically treated animals with DMBA followed by TPA. In this dataset, we additionally perform single-cell RNA-seq on back skin in mice treated exclusively with TPA as a control.
Project description:Skin constitutes the outer permeability barrier that protects the body from dehydration and a myriad of external assaults. Epidermal keratinocytes act as the first line of innate immune defense, and barrier defects underlie common inflammatory skin diseases. However, the molecular mechanisms that maintain barrier integrity when skin is under challenge to regulate the interplay between epidermal and immune cells are not fully understood. Here we report upregulated expression of transcriptional repressorencoding Ovol1 in epidermal cells of inflamed skin, and its functional importance in maintaining barrier integrity of physically or chemically challenged skin. Following stimulation with imiquimod, Ovol1-deficient mice exhibit significantly aggravated epidermal hyperplasia and psoriasis-like skin inflammation featuring persistent neutrophil accumulation. Using bulk and single-cell RNA-sequencing, we characterize molecular changes in epidermal, fibroblasts, and immune cells that reflect altered epidermal proliferation and differentiation and/or significantly enhanced inflammatory responses as consequences of Ovol1 deletion. We identify both proliferation/differentiation-regulating and neutrophil-attracting chemokine genes as candidate direct targets of Ovol1. Finally, we provide evidence for altered IL-1a signaling in the microenvironment of Ovol1- deficient inflamed skin that functionally contributes to neutrophil accumulation and epidermal hyperplasia. Collectively, our study demonstrates a protective role for an epidermally expressed, disease-linked transcription factor in coordinating robust barrier maintenance with suppression of skin inflammation.
