Literature DB >> 23039137

How do keratinizing disorders and blistering disorders overlap?

Takahiro Hamada1, Daisuke Tsuruta, Shunpei Fukuda, Norito Ishii, Kwesi Teye, Sanae Numata, Teruki Dainichi, Tadashi Karashima, Chika Ohata, Minao Furumura, Takashi Hashimoto.   

Abstract

Inherited keratinizing disorders are caused by mutations in the genes encoding cornified cell envelope proteins, enzymes and their inhibitors, adhesion molecules, cytoskeletal proteins and others in the epidermis. These molecules are known to regulate differentiation, proliferation and cell adhesions. Intriguingly, some keratinizing disorders show blistering skin lesions, while some inherited blistering disorders show abnormal keratinization. Therefore, hereditary keratinizing and blistering diseases are closely related and show overlapping genetic backgrounds. In this review, we overviewed keratinizing and blistering disorders in terms of overlapping of the two disease groups. Gene mutations in desmosomal components cause striate keratoderma, Naxos disease, epidermolytic palmoplantar keratoderma and plakophilin deficiency, which first show skin fragility and blisters and later hyperkeratosis. Gene mutations in hemidesmosomal components cause various forms of epidermolysis bullosa, some of which show hyperkeratosis on the nails, palms and soles, in addition to blister formation. Diseases with gene mutations in calcium pump proteins are Darier disease and Hailey-Hailey disease, which show clinicopathological overlaps and develop both keratinizing and blistering skin lesions. Finally, gene mutations in epidermal keratins cause epidermolysis bullosa simplex, epidermolytic ichthyosis, superficial epidermolytic ichthyosis, epidermolytic palmoplantar keratoderma and pachyonychia congenita/focal palmoplantar keratoderma, which show thickening of the palms and soles with underlying blister formation. In general, responsible proteins for diseases developing both keratinizing and blistering conditions are adhesion molecules, calcium pump proteins and keratins, but not connexins, cornified cell envelop proteins, enzymes or inhibitors. It is still unknown how particular keratinizing diseases develop blisters and vice versa.
© 2012 John Wiley & Sons A/S.

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Year:  2012        PMID: 23039137     DOI: 10.1111/exd.12021

Source DB:  PubMed          Journal:  Exp Dermatol        ISSN: 0906-6705            Impact factor:   3.960


  5 in total

1.  Chemical chaperone therapy, a new strategy for genetic skin fragility disorders.

Authors:  Jean Christopher Chamcheu; Imtiaz A Siddiqui; Hasan Mukhtar
Journal:  Exp Dermatol       Date:  2016-03       Impact factor: 3.960

2.  Oxidative stress and dysfunctional NRF2 underlie pachyonychia congenita phenotypes.

Authors:  Michelle L Kerns; Jill M C Hakim; Rosemary G Lu; Yajuan Guo; Andreas Berroth; Roger L Kaspar; Pierre A Coulombe
Journal:  J Clin Invest       Date:  2016-05-16       Impact factor: 14.808

3.  Novel sporadic and recurrent mutations in KRT5 and KRT14 genes in Polish epidermolysis bullosa simplex patients: further insights into epidemiology and genotype-phenotype correlation.

Authors:  K Wertheim-Tysarowska; M Ołdak; A Giza; A Kutkowska-Kaźmierczak; J Sota; D Przybylska; K Woźniak; D Śniegórska; K Niepokój; A Sobczyńska-Tomaszewska; A M Rygiel; R Płoski; J Bal; C Kowalewski
Journal:  J Appl Genet       Date:  2015-10-02       Impact factor: 3.240

4.  Bullous diseases caused by KRT1 gene mutations: from epidermolytic hyperkeratosis to a novel variant of epidermolysis bullosa simplex.

Authors:  Katarzyna Osipowicz; Katarzyna Wertheim-Tysarowska; Bartłomiej Kwiek; Ewa Jankowska; Monika Gos; Agnieszka Charzewska; Katarzyna Woźniak; Cezary Kowalewski
Journal:  Postepy Dermatol Alergol       Date:  2020-09-02       Impact factor: 1.837

5.  Keratinocyte detachment-differentiation connection revisited, or anoikis-pityriasi nexus redux.

Authors:  Tomohiro Banno; Miroslav Blumenberg
Journal:  PLoS One       Date:  2014-06-24       Impact factor: 3.240

  5 in total

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