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RNASeq analysis of skin from mice with keratinocyte-specific loss of MCPIP3.

ABSTRACT: RNASeq analysis of skin from mice with keratinocyte-specific loss of MCPIP3.

PROVIDER: PRJNA1223806 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32342561_1.fastq.gz	Fastqsanger.gz
	SRR32342561_2.fastq.gz	Fastqsanger.gz
	SRR32342562_1.fastq.gz	Fastqsanger.gz
	SRR32342562_2.fastq.gz	Fastqsanger.gz
	SRR32342563_1.fastq.gz	Fastqsanger.gz

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RNASeq analysis of skin from mice with keratinocyte-specific loss of MCPIP3.

Project description:Mice with keratinocyte-specific deletion of MCPIP3 (MCPIP3EKO) develop epidermal hyperplasia and abnormal differentiation. Loss of MCPIP3 function in murine keratinocytes leads to global changes of skin transcriptome. This study was funded by the National Science Centre grant number 2022/47/D/NZ3/01654 (to A. Lichawska-Cieslar).

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Conditional keratinocyte-specific ADAM17 knockout in mice alters skin homeostasis

Project description:This study investigates the role of ADAM17 (a disintegrin and metalloproteinase 17) in skin homeostasis. Here, we show that mice lacking ADAM17 in keratinocytes have a normal epidermal barrier and skin architecture at birth, but develop pronounced defects in epidermal barrier integrity soon after birth and chronic dermatitis as adults. The dysregulated expression of epidermal differentiation proteins becomes evident 2 days after birth, followed by transepidermal water loss and inflammatory immune cell infiltration. Our results identify a previously unappreciated critical role of the ADAM17/EGFR signaling axis in maintaining the homeostasis of the postnatal epidermal barrier. The genome-wide effects of ADAM17 deficiency were analyzed using Agilent Whole Mouse Genome microarrays. Conditional keratinocyte-specific ADAM17 knockout mice were generated by crossing Adam17flox/flox mice with keratin-14-Cre (Krt14-Cre) transgenic mice. Adam17flox/+Krt14-Cre mice were mated with Adam17flox/flox mice to generate pups of Adam17flox/flox Krt14-Cre positive (cKO) and Krt14-Cre negative (wild-type) control littermates. The genetic background was a mix of 129Sv and C57BL/6. As material, back skin tissue biopsies (postnatal day 10) from n = 2 wild-type skin and n = 2 ADAM17 epidermal KO skin (matched WT-cKO pairs from two different litters) were used in this study.

2012-06-20 | E-GEOD-38830 | biostudies-arrayexpress

Inducible keratinocyte-specific Mettl3-deficient mice develop spontaneous skin lesions

Project description:We conducted RNA sequencing analysis on skin tissues obtained from spontaneous inflammatory skin lesions in keratinocyte-specific Mettl3 knockout (K14CreERT2;Mettl3fl/fl) mice and their controls (Mettl3fl/fl). In brief, we observed spontaneous skin inflammation in the tail of K14CreERT2;Mettl3fl/fl mice 2-3 weeks following tamoxifen injection. The objective of this study was to investigate the impact and underlying mechanism of Mettl3 in epidermal keratinocytes regarding skin inflammation

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Inducible keratinocyte-specific Mettl3-deficient mice develop spontaneous skin lesions

Project description:Inducible keratinocyte-specific Mettl3-deficient mice develop spontaneous skin lesions

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Analysis of skin of keratinocyte-specific OTULIN-deficient mice by single-cell RNA-sequencing

Project description:In order to unravel the functional role of the linear deubiquitinase OTULIN, we performed single-cell RNA-sequencing on total skin of mice lacking OTULIN selectively in keratinocytes. Keratinocyte-specific OTULIN knock-out (KO) mice develop delineated inflammatory lesion. Through single-cell analysis on lesional and non-lesional skin of mice lacking OTULIN in keratinocytes, we could identify signalling pathways through which these inflammatory lesions appear, allowing us to get new insights on the molecular events that regulate skin homeostasis and mediate skin inflammation.

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Distinct roles of keratinocyte- and myeloid- MCPIP1 in maintaining skin homeostasis

Project description:The morphology of the skin changes upon depletion of MCPIP1 in cells of myeloid origin as well as in keratinocytes. The thicknesses of epidermal and hypodermal layers are significantly increased in mice with loss of epidermal MCPIP1, whereas loss of myeloid MCPIP1 exerts completely opposite effect. Both types of mice show contrary response to the stimulation with 12-O-tetradecanoylphorbol-13-acetate. Skin morphology and inflammatory phenotype of keratinocyte- and myeloid- double MCPIP1 knockout mice is similar to that of the single keratinocyte knockout of MCPIP1. In all, myeloid and epidermal MCPIP1 play significant but distinct roles in the modulation of skin-related processes. This study was funded by National Science Centre grant numbers 2020/37/N/NZ5/00575 (to Weronika Szukala) and 2021/41/B/NZ5/03601 (to Jolanta Jura)."

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Otulin inhibits RIPK1-mediated keratinocyte necroptosis to prevent skin inflammation in mice

Project description:Mice with epidermal keratinocyte specific knockout of OTULIN develop inflammatory skin disease. To study the inflammatory response we used Lexogen 3´mRNA sequencing to compare the gene expression profiles in the skin of OTULIN epidermis specific knockout and control mice.

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Effect of Sorafenib or Regorafenib on P63 Expression and Keratinocyte Differentiation in Human Skin

Project description:Skin toxicity is a frequently observed side effect in the era of "molecularly targeted therapies". Skin toxicity following administration of protein kinase inhibitors such as sorafenib, regorafenib, lapatinib, sunitinib, and others can be debilitating to the patient, resulting in dose reduction and discontinuation of treatment. The mechanisms of skin toxicity induced by targeted chemotherapy, such as sorafenib or regorafenib, are poorly understood. Further research is warranted to better understand the pathophysiology of drug-related skin toxicity in this setting and develop correction strategies. This study tests the hypothesis that sorafenib and regorafenib interfere with p63 expression and keratinocyte differentiation and skin remodeling. Eligible study participants will be evaluated clinically for evidence of skin toxicity during their visits to the outpatient Oncology clinics. Study participants will undergo skin biopsies before sorafenib or regorafenib treatment is initiated and once rash develops or 12 weeks into treatment with sorafenib or regorafenib. Skin biopsies will be performed in Oncology clinics by the study investigators and clinic support staff. Study participants will undergo both skin biopsies regardless of whether they develop a rash. In patients who develop a rash the most representative lesion will be biopsied. A normal appearing area of skin will be biopsied in participants who do not develop a rash.

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Analysis of skin of keratinocyte-specific OTULIN-deficient mice by single-cell RNA-sequencing

Project description:Analysis of skin of keratinocyte-specific OTULIN-deficient mice by single-cell RNA-sequencing

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Epidermal loss of PRMT5 leads to the emergence of an atypical basal keratinocyte-like cell population and defective skin stratification

Project description:During skin development, ectoderm-derived cells undergo precisely coordinated proliferation, differentiation, and adhesion to yield stratified epidermis. Disruptions in these processes can result in congenital anomalies including ectodermal dysplasia and harlequin ichthyosis. Protein Arginine Methyl Transferase 5 (PRMT5)—an enzyme responsible for methylating arginine residues in histones and other proteins—maintains progenitor status in germ and limb bud cells. Similarly, in vitro evidence suggests that PRMT5 prevents differentiation of basal keratinocytes, leading us to hypothesize that PRMT5 preserves the stem-cell phenotype of keratinocytes in vivo. To test this possibility, we generated conditional knockout (cKO) mice lacking Prmt5 in early ectoderm (E7.5), impacting the entire epidermis. Prmt5 cKOs exhibited gross skin defects, compromised skin barrier function, and reduced postnatal viability. Histological analyses revealed significant defects in epidermal stratification, without alterations in apoptosis or proliferation. Single-cell RNA and ATAC-seq analysis identified an atypical population of basal keratinocyte-like cells in Prmt5 cKOs, that exhibited a senescence-like program, characterized by increased Cdkn1a (p21), elevated senescence-associated secretory phenotype (SASP) molecules (Igfbp2), and decreased developmental transcription factor (Trp63) expression. Our findings suggest that PRMT5 prevents basal keratinocyte senescence by repressing Cdkn1a, shedding light on the epigenetic regulation of basal keratinocyte maintenance and senescence in congenital skin disorders.

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