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  • 1
    Electronic Resource
    Electronic Resource
    Copenhagen : Munksgaard International Publishers
    Experimental dermatology 9 (2000), S. 0 
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The study of mouse epidermal biology has been hampered by the lack of a good in vitro model for the culture of mouse keratinocytes which allowed the reconstruction of a fully differentiated epidermis. We adapted the Pruniéras' model, also called the Dead de-Epidermized Dermis model (DED), to mouse keratinocytes and showed that a neo-epidermis can be reconstructed exhibiting a complete differentiation program. We also used this model to culture transgenic mouse keratinocytes. We observed that transgene expression occurred in the correct location and that the neo-epidermis mimed previous in vivo observations obtained with integrin skin-targeted transgenic mice. Therefore, this model will be a powerful tool to further investigate normal mouse and transgenic keratinocyte biology.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Experimental dermatology 2 (1993), S. 0 
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract The wild-type tumor-suppressor TP53 gene encodes for a nuclear protein which has been shown to act as a transcriptional modulator. The cellular role of the p53 protein is the control of cell proliferation, particularly important in stressed cells. The TP53 gene is frequently mutated in sporadic and familial human cancers. Most transforming mutations localize in highly conserved domains of the gene and define hot-spot regions that have a certain degree of tissue specificity. Moreover, most mutations are point mutations and the type and localization of the nucleotide substitution may sometimes help in recognizing the carcinogenic agent. This is the case for C to T transitions at dipyrimidine sites induced by UV radiation in cutaneous epitheliomas. Inactivation of p53 protein can also occur through mechanisms other than genetic alteration, such as binding to viral or cellular proteins. Loss of wild-type TP53 function seems therefore to play a crucial role in cell transformation in human cancers, either during carcinogenesis or later in tumor progression.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    British journal of dermatology 153 (2005), S. 0 
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background  The origin of psoriasis, a chronic inflammatory skin disease involving keratinocyte proliferation, immune disturbances and complex inheritance, remains unknown. Human endogenous retroviruses (HERVs) are part of the normal human genome and their participation in the pathogenesis of various human diseases with complex genetic traits has been proposed. A possible role of HERVs in the induction of psoriasis was suggested many years ago. However, to date no study has searched for HERV expression in psoriasis.Objectives  To determine firstly, which HERV families are expressed in the psoriatic lesion and secondly, whether specific variants can be detected.Methods  HERV expression was analysed at the mRNA level after degenerated reverse transcription–polymerase chain reaction (RT–PCR) of retroviral pol sequences followed by sequencing. Screening for a specific variant was performed by RT–PCR on lesional and nonlesional psoriatic skin and compared with normal and atopic dermatitis skin.Results  We report the expression of three HERV families in psoriatic lesions, namely HERV-W, K and E. We then partially characterized a new endogenous retroviral variant, which was related to the ERV-9/HERV-W family. This sequence contains at least two open reading frames that could encode for a gag protein and a retroviral protease. The expression of this sequence was detected in 29 of 43 lesional psoriasis skin samples and rarely in normal (two of 21) or atopic dermatitis (three of 14) skin samples.Conclusions  In psoriatic lesions, HERV sequences of the W, K and E families are expressed and a new variant of the ERV-9/HERV-W family has been characterized. The possible role of HERV-related sequences in the pathogenesis of psoriasis is under investigation.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Experimental dermatology 6 (1997), S. 0 
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract In normal epidermis integrin expression is largely confined to the basal layer. However, during wound healing and in psoriatic lesions suprabasal expression is observed. Although the potential importance of suprabasal integrin expression in the pathogenesis of psoriasis has been established, the cause of suprabasal expression is unknown. We now describe changes in integrin expression that occur with time when normal human keratinocytes are grown on two types of dermal equivalent, de-epidermized dermis and collagen gels containing fibroblasts. We show that suprabasal integrin expression is correlated with suprabasal expression of the EGF receptor, but not with expression of keratin 10 or keratin 16. By quantitating the proportion of basal keratinocytes expressing the proliferation marker Ki-67 we could show that suprabasal integrin expression is correlated with high proliferative activity within the basal layer. Taken together with our earlier work, these results suggest that suprabasal integrin expression is linked to hyperproliferation and not to abnormal terminal differentiation or to inflammation; they also establish dermal equivalent cultures as useful experimental models with which to manipulate keratinocyte integrin expression.
    Type of Medium: Electronic Resource
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