Differentiation of organotypic epidermis in the presence of skin disease-linked dominant-negative cx26 mutants and knockdown cx26.

Differentiation of organotypic epidermis in the presence of skin disease-linked dominant-negative cx26 mutants and knockdown cx26. Research Abstract Details 

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Differentiation of organotypic epidermis in the presence of skin disease-linked dominant-negative cx26 mutants and knockdown cx26. Abstract Text:

Tamsin Thomas,Qing Shao,Dale W Laird,Tamsin Thomas,Qing Shao,Dale W Laird,

In this study, we chose a differentiation-competent rat epidermal keratinocyte (REK) cell line to examine the role of Cx26 and disease-linked Cx26 mutants in organotypic epidermal differentiation. First, we generated stable REK cell lines expressing three skin disease-linked mutants (G59A, D66H and R75W). Second, we used an RNAi approach to knock down the expression of Cx26 in REKs. Interestingly, the three-dimensional (3D) architecture of the organotypic epidermis altered the intracellular spatial distribution of the mutants in comparison to 2D cultured REKs, highlighting the importance of using organotypic cultures. Unexpectedly, the presence of disease-linked mutants or the overexpression of wild-type Cx26 had little effect on the differentiation of the organotypic epidermis as determined by the architecture of the epidermis, expression of molecular markers indicative of epidermis differentiation (keratin 10, keratin 14, involucrin, loricrin) and stratification/cornification of the epidermis. Likewise, organotypic epidermis continued to differentiate normally upon Cx26 knockdown. While Cx26 has been reported to be upregulated during wound healing, no reduction in wound closure was observed in 2D REK cultures that expressed loss-of-function, dominant Cx26 mutants. In conclusion, we demonstrate that gain or loss of Cx26 function does not disrupt organotypic epidermal differentiation and offer insights into why patients harboring Cx26 mutations do not frequently present with more severe disease that encompasses thin skin.

Differentiation of organotypic epidermis in the presence of skin disease-linked dominant-negative cx26 mutants and knockdown cx26. Publishing Authors By Initials

T Thomas,Q Shao,DW Laird,T Thomas,Q Shao,DW Laird,

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Differentiation of organotypic epidermis in the presence of skin disease-linked dominant-negative cx26 mutants and knockdown cx26. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: The Journal of membrane biology

VOLUME: 217

Page Numbers: 93-104

Journal Abbreviation: J. Membr. Biol.

ISSN: 0022-2631

DAY: 20

MONTH: 07

YEAR: 2007

Differentiation of organotypic epidermis in the presence of skin disease-linked dominant-negative cx26 mutants and knockdown cx26. Information

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LANGUAGE: eng

NlmUniqueID: 211301

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AFFILIATION: Department of Anatomy and Cell Biology, University of Western Ontario, London, N6A-5C1, Ontario, Canada, dale.laird@schulich.uwo.ca.

Country: United States

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MEDLINETA: J Membr Biol

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