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Biological therapy induces expression changes in Notch pathway in psoriasis

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Abstract

Psoriasis is a chronic inflammatory skin disease, characterized by hyperproliferation of keratinocytes and by skin infiltration of activated T cells. To date, the pathophysiology of psoriasis has not yet been fully elucidated. The Notch pathway plays a determinant role in cell fate determination, proliferation, differentiation, immune cell development and function. Many biological agents, used in the treatment of psoriasis, include TFN-α inhibitors, such as etanercept, adalimumab, and anti IL-12/IL-23 p40 antibody, such as ustekinumab. This study aimed to determine mRNA expression levels by real-time RT-PCR, and protein expression levels, analysed by Western blot and immunohistochemistry, of some components of the Notch pathway, such as NOTCH1, NOTCH2, JAGGED1, and HES1 after biological treatments in psoriatic patients. mRNA and protein levels of NOTCH1, NOTCH2, JAGGED1 and HES1 were upregulated in skin samples from untreated psoriatic patients compared with normal controls. Biological therapy showed to downregulate differently the protein expression levels of the molecules under study. Our study suggests that Notch pathway components might be a potential therapeutic target against psoriasis.

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Acknowledgments

This work received financial support from intramural grants provided by University of Catania, Italy.

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Correspondence to Fabio D’Amico.

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The authors declare that they have no conflict of interest.

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All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.

Additional information

F. D’Amico and M. C. Mazzarino are the senior authors who contributed equally to this study.

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Skarmoutsou, E., Trovato, C., Granata, M. et al. Biological therapy induces expression changes in Notch pathway in psoriasis. Arch Dermatol Res 307, 863–873 (2015). https://doi.org/10.1007/s00403-015-1594-7

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  • DOI: https://doi.org/10.1007/s00403-015-1594-7

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