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Loss of MPZL3 Function Causes Seborrheic Dermatitis-like Phenotype in Mice

ABSTRACT: Loss of MPZL3 Function Causes Seborrheic Dermatitis-like Phenotype in Mice

PROVIDER: PRJNA483074 | ENA |

REPOSITORIES: ENA

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Loss of MPZL3 Function Causes Seborrheic Dermatitis-like Phenotype in Mice

Project description:Seborrheic Dermatitis (SD) is a common inflammatory skin disorder. In this study, we demonstrated SD-like clinical features with associated histology in the Mpzl3 knockout(-/-) mice. Mpzl3-/- skin showed increased macrophage and CD4+ lymphocyte infiltration, however adaptive immunity was not required for the onset of skin inflammation. Furthermore, we detected epidermal barrier defects as suggested by increased dye permeability in Mpzl3-/- embryos and altered gene expression by microarray analysis in pup skin. Taken together, these findings suggest MPZL3 plays an essential role in epidermal differentiation and barrier function, and underscore the interplay between epidermal barrier and immunity in SD. The SD-like clinical and histologic features in the Mpzl3-/- mice also resemble those in patients carrying a frame-shift mutation in ZNF750, a key regulator of epidermal differentiation and a transcriptional activator of the MPZL3 gene. Therefore, we conclude that the ZNF750/MPZL3 pathway plays a critical role in the pathogenesis of SD, and a better understanding of skin inflammation and barrier restoration in the Mpzl3-/- mice will provide insight into the pathogenesis and treatment/prevention of recurrent SD.

2018-07-27 | GSE117755 | GEO

Loss of MPZL3 function causes seborrhoeic dermatitis-like phenotype in mice.

Project description: Not available

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Genomic profiling of the overlap phenotype between psoriasis and atopic dermatitis

Project description:Clinical overlaps between psoriasis and atopic dermatitis are sometimes undiscernible, and there is no consensus whether to treat the overlap phenotype as psoriasis or atopic dermatitis. We enrolled patients diagnosed with either psoriasis or atopic dermatitis, and clinically re-stratified them into classic psoriasis, classic atopic dermatitis, and the overlap phenotype between psoriasis and atopic dermatitis. We compared gene expression profiles of lesional and nonlesional skin biopsy tissues between the three comparison groups. Global mRNA expression and T-cell subset cytokine expression in the skin of the overlap phenotype were consistent with the profiles of psoriasis and different from the profiles of atopic dermatitis. Unsupervised k-means clustering indicated that the best number of distinct clusters for the total population of the three comparison groups was two, and the two clusters of psoriasis and atopic dermatitis were differentiated by gene expression. Our study suggests that clinical overlap phenotype between psoriasis and atopic dermatitis has dominant molecular features of psoriasis, and genomic biomarkers can differentiate psoriasis and atopic dermatitis at molecular levels in patients with a spectrum of psoriasis and atopic dermatitis.

2023-06-24 | GSE182740 | GEO

Loss of function of CENH3 causes genome instability in soybean

Project description:Loss of function of CENH3 causes genome instability in soybean

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Epidermal Nbn deletion causes premature hair loss and a phenotype resembling psoriasiform dermatitis.

Project description:Nijmegen Breakage Syndrome is a disease caused by NBN mutations. Here, we report a novel function of Nbn in skin homeostasis. We found that Nbn deficiency in hair follicle (HF) progenitors promoted increased DNA damage signaling, stimulating p16Ink4a up-regulation, Trp53 stabilization and cytokines secretion leading to HF-growth arrest and hair loss. At later stages, the basal keratinocytes layer exhibited also enhanced DNA damage response but in contrast to the one in HF progenitor was not associated with pro-inflammatory cytokines expression, but rather increased proliferation, lack of differentiation and immune response resembling psoriasiform dermatitis. Simultaneous Nbn and Trp53 inactivation significantly exacerbated this phenotype, due to the lack of inhibition of pro-inflammatory cytokines secretion by Trp53. Altogether, we demonstrated novel functions of Nbn in HF maintenance and prevention of skin inflammation and we provide a mechanistic explanation that links cell intrinsic DNA maintenance with large scale morphological tissue alterations.

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ZNF750 loss in junctional zone of hair follicle and sebaceous gland leads to severe seborrheic-like psoriasiform dermatitis [day 50]

Project description:ZNF750 loss in junctional zone of hair follicle and sebaceous gland leads to severe seborrheic-like psoriasiform dermatitis [day 50]

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ZNF750 loss in junctional zone of hair follicle and sebaceous gland leads to severe seborrheic-like psoriasiform dermatitis [day 36]

Project description:ZNF750 loss in junctional zone of hair follicle and sebaceous gland leads to severe seborrheic-like psoriasiform dermatitis [day 36]

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Genomic profiling of the overlap phenotype between psoriasis and atopic dermatitis

Project description:Genomic profiling of the overlap phenotype between psoriasis and atopic dermatitis

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Loss of protein association causes cardiolipin degradation in Barth syndrome

Project description:Loss of protein association causes cardiolipin degradation in Barth syndrome

2016-03-22 | MSV000079600 | MassIVE

Mind Bomb 2 limits inflammatory dermatitis in Sharpin mutant mice independently of cell death

Project description:Skin inflammation is a complex process implicated in various dermatological disorders. The chronic proliferative dermatitis (cpd) phenotype driven by the cpd mutation (cpdm) in the Sharpin gene is characterized by dermal inflammation and epidermal abnormalities. TNF and caspase-8-driven cell death causes the pathogenesis of Sharpincpdm mice, however, the role of MIB2, a pro-survival E3 ubiquitin ligase involved in TNF-signalling, in skin inflammation remains unknown. Here we demonstrate that MIB2 antagonises inflammatory dermatitis in the context of the cpd mutation. Surprisingly, the role of MIB2 in limiting skin inflammation is independent of its known pro-survival function and E3 ligase activity. Instead, MIB2 enhances the production of wound healing molecules, G-CSF and Eotaxin, within the skin. This discovery advances our comprehension of inflammatory cytokines and chemokines involved in cpdm pathogenesis, and highlights the significance of MIB2 in inflammatory skin disease that is independent of its ability to regulate TNF-induced cell death.

2024-01-25 | PXD045850 | Pride

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