Mind bomb 2 limits inflammatory dermatitis in Sharpin mutant mice independently of cell death
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. Tumour necrosis factor (TNF) and casp...
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Published in | PNAS nexus Vol. 3; no. 1; p. pgad438 |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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Oxford University Press
01.01.2024
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Abstract | 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. Tumour necrosis factor (TNF) and caspase-8-driven cell death causes the pathogenesis of
mice; however, the role of mind bomb 2 (MIB2), a pro-survival E3 ubiquitin ligase involved in TNF signaling, in skin inflammation remains unknown. Here, we demonstrate that MIB2 antagonizes 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, granulocyte colony-stimulating factor, and Eotaxin, within the skin. This discovery advances our comprehension of inflammatory cytokines and chemokines associated with cpdm pathogenesis and highlights the significance of MIB2 in inflammatory skin disease that is independent of its ability to regulate TNF-induced cell death. |
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AbstractList | 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. Tumour necrosis factor (TNF) and caspase-8-driven cell death causes the pathogenesis of [Sharpin.sup.cpdm] mice; however, the role of mind bomb 2 (MIB2), a pro-survival E3 ubiquitin ligase involved in TNF signaling, in skin inflammation remains unknown. Here, we demonstrate that MIB2 antagonizes 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, granulocyte colony-stimulating factor, and Eotaxin, within the skin. This discovery advances our comprehension of inflammatory cytokines and chemokines associated with cpdm pathogenesis and highlights the significance of MIB2 in inflammatory skin disease that is independent of its ability to regulate TNF-induced cell death. Keywords: mind bomb 2, Sharpin, cpdm, dermatitis, TNF 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. Tumour necrosis factor (TNF) and caspase-8-driven cell death causes the pathogenesis of Sharpin cpdm mice; however, the role of mind bomb 2 (MIB2), a pro-survival E3 ubiquitin ligase involved in TNF signaling, in skin inflammation remains unknown. Here, we demonstrate that MIB2 antagonizes 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, granulocyte colony-stimulating factor, and Eotaxin, within the skin. This discovery advances our comprehension of inflammatory cytokines and chemokines associated with cpdm pathogenesis and highlights the significance of MIB2 in inflammatory skin disease that is independent of its ability to regulate TNF-induced cell death. 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. Tumour necrosis factor (TNF) and caspase-8-driven cell death causes the pathogenesis of [Sharpin.sup.cpdm] mice; however, the role of mind bomb 2 (MIB2), a pro-survival E3 ubiquitin ligase involved in TNF signaling, in skin inflammation remains unknown. Here, we demonstrate that MIB2 antagonizes 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, granulocyte colony-stimulating factor, and Eotaxin, within the skin. This discovery advances our comprehension of inflammatory cytokines and chemokines associated with cpdm pathogenesis and highlights the significance of MIB2 in inflammatory skin disease that is independent of its ability to regulate TNF-induced cell death. 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. Tumour necrosis factor (TNF) and caspase-8-driven cell death causes the pathogenesis of Sharpincpdm mice; however, the role of mind bomb 2 (MIB2), a pro-survival E3 ubiquitin ligase involved in TNF signaling, in skin inflammation remains unknown. Here, we demonstrate that MIB2 antagonizes 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, granulocyte colony-stimulating factor, and Eotaxin, within the skin. This discovery advances our comprehension of inflammatory cytokines and chemokines associated with cpdm pathogenesis and highlights the significance of MIB2 in inflammatory skin disease that is independent of its ability to regulate TNF-induced cell death. 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. Tumour necrosis factor (TNF) and caspase-8-driven cell death causes the pathogenesis of mice; however, the role of mind bomb 2 (MIB2), a pro-survival E3 ubiquitin ligase involved in TNF signaling, in skin inflammation remains unknown. Here, we demonstrate that MIB2 antagonizes 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, granulocyte colony-stimulating factor, and Eotaxin, within the skin. This discovery advances our comprehension of inflammatory cytokines and chemokines associated with cpdm pathogenesis and highlights the significance of MIB2 in inflammatory skin disease that is independent of its ability to regulate TNF-induced cell death. |
Audience | Academic |
Author | Yousef, Jumana Dagley, Laura F Vince, James E Bandala-Sanchez, Esther Anderton, Holly Kueh, Andrew J Simpson, Daniel S Cobbold, Simon A Vaibhav, Vineet Herold, Marco J Feltham, Rebecca Silke, John |
Author_xml | – sequence: 1 givenname: Daniel S orcidid: 0000-0002-6248-427X surname: Simpson fullname: Simpson, Daniel S organization: Department of Medical Biology, University of Melbourne, Parkville, Melbourne, VIC 3050, Australia – sequence: 2 givenname: Holly orcidid: 0000-0003-3913-9686 surname: Anderton fullname: Anderton, Holly organization: Department of Medical Biology, University of Melbourne, Parkville, Melbourne, VIC 3050, Australia – sequence: 3 givenname: Jumana orcidid: 0000-0002-2364-6299 surname: Yousef fullname: Yousef, Jumana organization: Department of Medical Biology, University of Melbourne, Parkville, Melbourne, VIC 3050, Australia – sequence: 4 givenname: Vineet surname: Vaibhav fullname: Vaibhav, Vineet organization: Department of Medical Biology, University of Melbourne, Parkville, Melbourne, VIC 3050, Australia – sequence: 5 givenname: Simon A orcidid: 0000-0002-9927-8998 surname: Cobbold fullname: Cobbold, Simon A organization: Department of Medical Biology, University of Melbourne, Parkville, Melbourne, VIC 3050, Australia – sequence: 6 givenname: Esther orcidid: 0000-0003-3875-8872 surname: Bandala-Sanchez fullname: Bandala-Sanchez, Esther organization: Department of Medical Biology, University of Melbourne, Parkville, Melbourne, VIC 3050, Australia – sequence: 7 givenname: Andrew J surname: Kueh fullname: Kueh, Andrew J organization: School of Cancer Medicine, La Trobe University, Heidelberg, VIC 3084, Australia – sequence: 8 givenname: Laura F orcidid: 0000-0003-4171-3712 surname: Dagley fullname: Dagley, Laura F organization: Department of Medical Biology, University of Melbourne, Parkville, Melbourne, VIC 3050, Australia – sequence: 9 givenname: Marco J orcidid: 0000-0001-7539-7581 surname: Herold fullname: Herold, Marco J organization: School of Cancer Medicine, La Trobe University, Heidelberg, VIC 3084, Australia – sequence: 10 givenname: John orcidid: 0000-0002-7611-5774 surname: Silke fullname: Silke, John organization: Department of Medical Biology, University of Melbourne, Parkville, Melbourne, VIC 3050, Australia – sequence: 11 givenname: James E orcidid: 0000-0001-7166-2798 surname: Vince fullname: Vince, James E organization: Department of Medical Biology, University of Melbourne, Parkville, Melbourne, VIC 3050, Australia – sequence: 12 givenname: Rebecca orcidid: 0000-0001-8376-6869 surname: Feltham fullname: Feltham, Rebecca organization: Department of Medical Biology, University of Melbourne, Parkville, Melbourne, VIC 3050, Australia |
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Keywords | cpdm dermatitis mind bomb 2 TNF Sharpin |
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SubjectTerms | Analysis Biological, Health, and Medical Sciences Cell death Dermatitis Genetic aspects Identification and classification Inflammation Properties Skin Ubiquitin |
Title | Mind bomb 2 limits inflammatory dermatitis in Sharpin mutant mice independently of cell death |
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