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ZEB2-transgene expression in the epidermis compromises the integrity of the epidermal barrier through the repression of different tight junction proteins

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Abstract
Epithelial homeostasis within the epidermis is maintained by means of multiple cell-cell adhesion complexes such as adherens junctions, tight junctions, gap junctions, and desmosomes. These complexes co-operate in the formation and the regulation of the epidermal barrier. Disruption of the epidermal barrier through the deregulation of the above complexes is the cause behind a number of skin disorders such as psoriasis, dermatitis, keratosis, and others. During epithelial-to-mesenchymal transition (EMT), epithelial cells lose their adhesive capacities and gain mesenchymal properties. ZEB transcription factors are key inducers of EMT. In order to gain a better understanding of the functional role of ZEB2 in epidermal homeostasis, we generated a mouse model with conditional overexpression of Zeb2 in the epidermis. Our analysis revealed that Zeb2 expression in the epidermis leads to hyperproliferation due to the combined downregulation of different tight junction proteins compromising the epidermal barrier. Using two epidermis-specific in vivo models and in vitro promoter assays, we identified occludin as a new Zeb2 target gene. Immunohistological analysis performed on human skin biopsies covering various pathogeneses revealed ZEB2 expression in the epidermis of pemphigus vulgaris. Collectively, our data support the notion for a potential role of ZEB2 in intracellular signaling of this disease.
Keywords
OCCLUDIN, SKIN, SIP1, PROGRESSION, INSIGHTS, CANCER INITIATION, E-CADHERIN, EPITHELIAL-MESENCHYMAL TRANSITION, Skin, Tight junctions, ZEB2, EMT, DISEASE, SHEET FORMATION

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Citation

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MLA
Tatari, Marianthi, Bram De Craene, Bieke Soen, et al. “ZEB2-transgene Expression in the Epidermis Compromises the Integrity of the Epidermal Barrier Through the Repression of Different Tight Junction Proteins.” CELLULAR AND MOLECULAR LIFE SCIENCES 71.18 (2014): 3599–3609. Print.
APA
Tatari, M., De Craene, B., Soen, B., Taminau, J., Vermassen, P., Goossens, S., Haigh, K., et al. (2014). ZEB2-transgene expression in the epidermis compromises the integrity of the epidermal barrier through the repression of different tight junction proteins. CELLULAR AND MOLECULAR LIFE SCIENCES, 71(18), 3599–3609.
Chicago author-date
Tatari, Marianthi, Bram De Craene, Bieke Soen, Joachim Taminau, Petra Vermassen, Steven Goossens, Katharina Haigh, et al. 2014. “ZEB2-transgene Expression in the Epidermis Compromises the Integrity of the Epidermal Barrier Through the Repression of Different Tight Junction Proteins.” Cellular and Molecular Life Sciences 71 (18): 3599–3609.
Chicago author-date (all authors)
Tatari, Marianthi, Bram De Craene, Bieke Soen, Joachim Taminau, Petra Vermassen, Steven Goossens, Katharina Haigh, Silvia Cazzola, Jo Lambert, Danny Huylebroeck, Jody Haigh, and Geert Berx. 2014. “ZEB2-transgene Expression in the Epidermis Compromises the Integrity of the Epidermal Barrier Through the Repression of Different Tight Junction Proteins.” Cellular and Molecular Life Sciences 71 (18): 3599–3609.
Vancouver
1.
Tatari M, De Craene B, Soen B, Taminau J, Vermassen P, Goossens S, et al. ZEB2-transgene expression in the epidermis compromises the integrity of the epidermal barrier through the repression of different tight junction proteins. CELLULAR AND MOLECULAR LIFE SCIENCES. 2014;71(18):3599–609.
IEEE
[1]
M. Tatari et al., “ZEB2-transgene expression in the epidermis compromises the integrity of the epidermal barrier through the repression of different tight junction proteins,” CELLULAR AND MOLECULAR LIFE SCIENCES, vol. 71, no. 18, pp. 3599–3609, 2014.
@article{5732564,
  abstract     = {{Epithelial homeostasis within the epidermis is maintained by means of multiple cell-cell adhesion complexes such as adherens junctions, tight junctions, gap junctions, and desmosomes. These complexes co-operate in the formation and the regulation of the epidermal barrier. Disruption of the epidermal barrier through the deregulation of the above complexes is the cause behind a number of skin disorders such as psoriasis, dermatitis, keratosis, and others. During epithelial-to-mesenchymal transition (EMT), epithelial cells lose their adhesive capacities and gain mesenchymal properties. ZEB transcription factors are key inducers of EMT. In order to gain a better understanding of the functional role of ZEB2 in epidermal homeostasis, we generated a mouse model with conditional overexpression of Zeb2 in the epidermis. Our analysis revealed that Zeb2 expression in the epidermis leads to hyperproliferation due to the combined downregulation of different tight junction proteins compromising the epidermal barrier. Using two epidermis-specific in vivo models and in vitro promoter assays, we identified occludin as a new Zeb2 target gene. Immunohistological analysis performed on human skin biopsies covering various pathogeneses revealed ZEB2 expression in the epidermis of pemphigus vulgaris. Collectively, our data support the notion for a potential role of ZEB2 in intracellular signaling of this disease.}},
  author       = {{Tatari, Marianthi and De Craene, Bram and Soen, Bieke and Taminau, Joachim and Vermassen, Petra and Goossens, Steven and Haigh, Katharina and Cazzola, Silvia and Lambert, Jo and Huylebroeck, Danny and Haigh, Jody and Berx, Geert}},
  issn         = {{1420-682X}},
  journal      = {{CELLULAR AND MOLECULAR LIFE SCIENCES}},
  keywords     = {{OCCLUDIN,SKIN,SIP1,PROGRESSION,INSIGHTS,CANCER INITIATION,E-CADHERIN,EPITHELIAL-MESENCHYMAL TRANSITION,Skin,Tight junctions,ZEB2,EMT,DISEASE,SHEET FORMATION}},
  language     = {{eng}},
  number       = {{18}},
  pages        = {{3599--3609}},
  title        = {{ZEB2-transgene expression in the epidermis compromises the integrity of the epidermal barrier through the repression of different tight junction proteins}},
  url          = {{http://dx.doi.org/10.1007/s00018-014-1589-0}},
  volume       = {{71}},
  year         = {{2014}},
}

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