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Sökning: WFRF:(Szell M)

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1.
  • Farkas, A, et al. (författare)
  • Dithranol upregulates IL-10 receptors on the cultured human keratinocyte cell line HaCaT.
  • 2001
  • Ingår i: Inflammation Research. - : Springer Science and Business Media LLC. - 1023-3830 .- 1420-908X. ; 50:1, s. 44-9
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: Dithranol is highly effective in the treatment of psoriasis, however its mode of action is still not well known. Since interleukin-8 and interleukin-10 are involved in the pathogenesis of psoriasis, the aim of our study was to investigate the effect of dithranol on interleukin-8, interleukin-10 mRNA production and interleukin-10 receptor expression of the HaCaT keratinocyte cell line which is commonly used in experiments examining the effects of therapeutic drugs on keratinocytes.MATERIALS AND METHODS: Cultured HaCaT cells were treated with 0.1-0.5 microg/ml dithranol for 30 minutes. After 2 and 4 h total cellular RNA isolated from HaCaT cells was reverse transcribed (RT) to cDNA which was subjected to polymerase chain reaction (PCR) with specific primer pairs for interleukin-8, interleukin-10 and interleukin-10 receptor. For immunohistochemistry cultured HaCaT cells were stained with a monoclonal antibody against the human interleukin-10 receptor.RESULTS: Our results showed that dithranol treatment did not change the highly elevated level of interleukin-8 mRNA of HaCaT cells. Interleukin-10 mRNA signal with RT-PCR could not be detected in HaCaT cells. Depending on the concentration dithranol increased the mRNA production of interleukin-10 receptors in HaCaT cells. This dithranol induced dose dependent upregulation of IL-10 receptors in HaCaT cells was also observed on the protein level using immunohistochemistry.CONCLUSIONS: Since the interleukin-10 receptor expression of keratinocytes in psoriatic lesional skin is downregulated, the dithranol induced upregulation of the receptor in our model system might help to reveal the therapeutic action of the drug.
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3.
  • Peltonen, Sirkku, 1964, et al. (författare)
  • Celebrating the 50th Anniversary of ESDR.
  • 2020
  • Ingår i: The Journal of investigative dermatology. - : Elsevier BV. - 1523-1747 .- 0022-202X. ; 140:9S
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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4.
  • Pivarcsi, A, et al. (författare)
  • Serum factors regulate the expression of the proliferation-related genes alpha5 integrin and keratin 1, but not keratin 10, in HaCaT keratinocytes.
  • 2001
  • Ingår i: Archives of Dermatological Research. - : Springer Science and Business Media LLC. - 0340-3696 .- 1432-069X. ; 293:4, s. 206-13
  • Tidskriftsartikel (refereegranskat)abstract
    • In the highly coordinated programme of gene expression during keratinocyte proliferation and differentiation, alpha5 integrin and keratins 1 and 10 (K1/K10) may play important regulatory roles. We were interested in seeing whether, in continuously growing, immortalized HaCaT keratinocytes, similar to normal keratinocytes, the expression of alpha5 integrin and K1/K10 was related to cell proliferation and differentiation. After release from cell quiescence the expression of alpha5 integrin, both at the mRNA and protein levels, was upregulated in the cells. At the same time, K1/K10 mRNA and protein expression decreased dramatically, while the mRNA for D1 cyclin became detectable, and the cells became highly proliferative. These findings indicate that alpha5 integrin and K1/K10 are involved in the regulation of HaCaT proliferation and differentiation, as in normal keratinocytes. However, HaCaT cells are different from normal keratinocytes in their ability to lose K1/K10 expression. There is no evidence that the expression of K1/K10 can be reversed in normal keratinocytes. This ability of dedifferentiation might be a unique feature of HaCaT cells and may be a key component of their immortalized nature. We also found that serum factors regulate mRNA expression of alpha5 integrin and K1, but not of K10, in HaCaT cells. This information could be relevant to the understanding of normal epidermal differentiation.
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