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Sökning: L773:0340 3696 OR L773:1432 069X

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5.
  • Assarsson, Malin, et al. (författare)
  • Narrowband UVB treatment induces expression of WNT7B, WNT10B and TCF7L2 in psoriasis skin
  • 2019
  • Ingår i: Archives of Dermatological Research. - : SPRINGER. - 0340-3696 .- 1432-069X. ; 311:7, s. 535-544
  • Tidskriftsartikel (refereegranskat)abstract
    • WNT/beta-catenin signaling pathways play a pivotal role in the human immune defense against infections and in chronic inflammatory conditions as psoriasis. Wnt gene alterations are linked to known comorbidities of psoriasis as obesity, diabetes and Crohns disease. The objective of this study was to investigate WNT7B, WNT10B, WNT16 and TCF7L2 gene and protein expression in lesional and non-lesional skin and in the peripheral blood of patients with chronic plaque psoriasis compared with healthy individuals. To investigate the effect of narrowband UVB radiation, expression of these genes were analyzed before and after narrowband UVB treatment. Associations between single nucleotide polymorphisms for WNT7B, WNT10B, WNT16 and TCF7L2 genes and psoriasis were tested. Our results show significantly decreased WNT7B, WNT10B and TCF7L2 gene expression in lesional skin compared with non-lesional skin and healthy controls. Narrowband UVB treatment significantly increased expression of these genes in lesional skin. Immunohistochemistry shows increased WNT16 expression in lesional skin. No significant differences in allele or genotype frequencies for Wnt or TCF7L2 gene polymorphisms were found between patient and control group. This study shows for the first time significant UVB induced upregulation of WNT7B, WNT10B and TCF7L2 in patients with psoriasis and suggests a potential role of these genes in psoriasis pathogenesis.
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  • Björntorp Mark, Elisabeth, 1964, et al. (författare)
  • Expression of genes involved in the regulation of p16 in psoriatic involved skin
  • 2006
  • Ingår i: Arch Dermatol Res. - : Springer Science and Business Media LLC. - 0340-3696. ; 297:10, s. 459-67
  • Tidskriftsartikel (refereegranskat)abstract
    • It has been suggested that the up-regulation of the tumour suppressor p16 gene and induction of senescence protect the phenotype of psoriatic involved skin from malignant transformation. On the other hand, Id1, which is inversely correlated with p16 has been shown to be up-regulated in psoriatic involved skin. To test the hypothesis that there may be an altered regulation of p16 in psoriatic involved skin, we have measured genes involved in the Igf-1 receptor signalling through the Ras/MAPK cascade. Igf-1R, IGFBP3, hRas, Ets2, JunB, Egr-1, Id1, MIDA1 and p16 gene expressions were measured using quantitative real-time PCR in total RNA isolated from punch biopsies from psoriatic involved (n = 9) and uninvolved skin (n = 9) and from cutaneous squamous cell cancer (SCC) involved (n = 8) and uninvolved skin (n = 8). The IGFBP3, hRas, JunB, Egr-1, Id1 and MIDA1 genes were up-regulated in psoriatic involved skin compared with uninvolved skin. The p16, JunB and MIDA1 genes were up-regulated in SCC involved skin compared with uninvolved skin. Our results indicate that there may be a balance between the proliferation and induction of senescence in psoriasis. This balance may vary and the psoriatic involved skin represented in this study appears to be in a proliferative state rather than senescence. Furthermore, we suggest that the noted up-regulation of JunB, which has been shown to up-regulate p16, in combination with the previously reported elevation of p16 expression in psoriatic involved skin, may indicate activation of a pathway by which JunB may protect the psoriatic plaque by inducing p16 in an event of malignant stress.
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  • Bock (Seifert), Oliver, et al. (författare)
  • Quality of life of patients with keloid and hypertrophic scarring
  • 2006
  • Ingår i: Archives of dermatological research. - : Springer Science and Business Media LLC. - 0340-3696 .- 1432-069X. ; 297:10, s. 433-438
  • Tidskriftsartikel (refereegranskat)abstract
    • Keloid and hypertrophic scarring represent chronic disfiguring dermatoses with a high resistance to therapy. The aim of our study was to assess for the first time the quality of life of patients with hypertrophic scars and keloids, because they suffer from quality of life impairment as much as patients with other chronic skin diseases. An item-pool was created modifying and supplementing the items of the Questionnaire on Experience with Skin Complaints. This questionnaire was distributed to 100 outpatients with keloids and hypertrophic scars. A factor analysis was used to identify the underlying dimensions. Two scales (psychological and physical impairment) of the questionnaire with nine and five items, respectively, were established. Test–retest reliability of the questionnaire was excellent (corr>0.9). Good validity was suggested by the correlation of physical impairment with pain (P≤0.001), pruritus (P<0.001), and the amount of restriction of mobility (P<0.001). The psychological scale was associated with pain and restriction of mobility, although the correlations were lower. This study demonstrates for the first time an impairment of quality of life in a large group of patients with keloid and hypertrophic scarring.
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  • Buraczewska, Izabela, et al. (författare)
  • Long-term treatment with moisturizers affects the mRNA levels of genes involved in keratinocyte differentiation and desquamation
  • 2009
  • Ingår i: Archives of Dermatological Research. - : Springer Science and Business Media LLC. - 0340-3696 .- 1432-069X. ; 301:2, s. 175-181
  • Tidskriftsartikel (refereegranskat)abstract
    • In a recent study, we showed that long-term treatment with two different moisturizers affected TEWL in opposite directions. Therefore, we decided to examine the effect of these moisturizers on the cellular and molecular level. In a randomized controlled study on 20 volunteers, epidermal mRNA expression of genes essential for keratinocyte differentiation and desquamation after a 7-week treatment with two moisturizers was analyzed. Treatment with one test moisturizer increased gene expression of involucrin, transglutaminase 1, kallikrein 5, and kallikrein 7, while the other moisturizer affected only expression of cyclin-dependent kinase inhibitor 1A. Thus, moisturizers are able to modify the skin barrier function and change the mRNA expression of certain epidermal genes. Since the type of influence depends on the composition of the moisturizer, these should be tailored in accordance with the requirement of the barrier of each individual patient, which merits further investigations.
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10.
  • Buraczewska, Izabela, et al. (författare)
  • Moisturizers change the mRNA expression of enzymes synthesizing skin barrier lipids
  • 2009
  • Ingår i: Archives of Dermatological Research. - : Springer Science and Business Media LLC. - 0340-3696 .- 1432-069X. ; 301:8, s. 587-594
  • Tidskriftsartikel (refereegranskat)abstract
    • In a previous study, 7-week treatment of normal human skin with two test moisturizers, Complex cream and Hydrocarbon cream, was shown to affect mRNA expression of certain genes involved in keratinocyte differentiation. Moreover, the treatment altered transepidermal water loss (TEWL) in opposite directions. In the present study, the mRNA expression of genes important for formation of barrier lipids, i.e., cholesterol, free fatty acids and ceramides, was examined. Treatment with Hydrocarbon cream, which increased TEWL, also elevated the gene expression of GBA, SPTLC2, SMPD1, ALOX12B, ALOXE3, and HMGCS1. In addition, the expression of PPARG was decreased. On the other hand, Complex cream, which decreased TEWL, induced only the expression of PPARG, although not confirmed at the protein level. Furthermore, in the untreated skin, a correlation between the mRNA expression of PPARG and ACACB, and TEWL was found, suggesting that these genes are important for the skin barrier homeostasis. The observed changes further demonstrate that long-term treatment with certain moisturizers may induce dysfunctional skin barrier, and as a consequence several signaling pathways are altered.
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