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World J Dermatol. Aug 2, 2014; 3(3): 50-57
Published online Aug 2, 2014. doi: 10.5314/wjd.v3.i3.50
What have we learned about non-involved psoriatic skin from large-scale gene expression studies?
Eszter Szlavicz, Kornelia Szabo, Zsuzsanna Bata-Csorgo, Lajos Kemeny, Marta Szell
Eszter Szlavicz, Zsuzsanna Bata-Csorgo, Lajos Kemeny, Department of Dermatology and Allergology, University of Szeged, H-6720 Szeged, Hungary
Kornelia Szabo, Zsuzsanna Bata-Csorgo, Lajos Kemeny, Marta Szell, Dermatological Research Group of the Hungarian Academy of Sciences, University of Szeged, H-6720 Szeged, Hungary
Marta Szell, Department of Medical Genetics, the University of Szeged, H-6720 Szeged, Hungary
Author contributions: Szlavicz E contributed to experimental work on the splice regulatory genes, review of previous papers, writing of the manuscript; Szabo K contributed to experimental work with the microarray-identified genes; Bata-Csorgo Zs contributed to co-ordination of the clinical aspects of the work, collection of skin specimen; Kemeny L contributed to co-ordination of the clinical and experimental aspects of psoriasis research; Szell M contributed to experimental work on the differential-display-identified genes, supervising experimental aspects of the review.
Supported by OTKA NK77434, OTKA K 83277, OTKA K105985 and TÁMOP-4.2.2.A-11/1/KONV, TÁMOP-4.2.2-B-10/1-2010-0012; the Bolyai Foundation of the Hungarian Academy of Sciences (to Kornelia Szabo)
Correspondence to: Eszter Szlavicz, MD, Department of Dermatology and Allergology, University of Szeged, Koranyi fasor 6, H-6720 Szeged, Hungary. szlavicz.eszter@gmail.com
Telephone: +36-62-545277 Fax: +36-62-545954
Received: December 29, 2013
Revised: May 22, 2014
Accepted: May 28, 2014
Published online: August 2, 2014
Core Tip

Core tip: Large-scale gene expression studies, including differential display and microarray, have provided valuable data on the molecular background of psoriasis pathogenesis. This review summarizes the most important results of the available literature and our large-scale gene expression studies obtained from the clinically non-involved psoriatic skin: we identified the EDA+ fibronectin splice variant as an autocrine proliferation signal for psoriatic hyperproliferative keratinocytes and PRINS, a long non-coding regulatory RNA. We believe that the characterization of new candidate genes and proteins might establish new therapeutic approaches, which may allow treatment of already existing psoriatic lesions as well as non-involved psoriatic skin by affecting molecular aberrancies, and may lead to the development of prophylactic interventions.