Splicing regulation disturbances in psoriasis pathogenesis

Szlávicz, Eszter and Szabó, Kornélia and Bata-Csörgő, Zsuzsanna and Bebes, Attila and Francziszti, László and Dobozy, Attila and Groma, Gergely and Kemény, Lajos and Széll, Márta (2014) Splicing regulation disturbances in psoriasis pathogenesis. JOURNAL OF INVESTIGATIVE DERMATOLOGY, 134 (Suppl.). p. 61. ISSN 0022-202X

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Abstract

In a recently performed cDNA microarray experiment we identified three splicing regulators (serine/arginine-rich splicing factor 18 (SFRS18), peptydilpropyl isomerase G (PPIG), luc-7 like3 (LUC7L3) that where differentially expressed in response to T-lymphokines in healthy and psoriatic non-involved epidermis samples. We and others have previously shown that the oncofetal splice variant of fibronectin - the isoform containing the EDA domain (EDA+) - is overexpressed in psoriatic non-involved epidermis. In this study we investigated whether SFRS18, LUC7L3 and PPIG are able to alter the ratio of the normal (EDA-) and psoriasis-associated (EDA+) variant. To this aim the expressions of the splicing regulators were silenced in immortalized keratinocytes (HPV-KER). We found that the EDA+/EDA- ratio was altered upon silencing of LUC7L3 and PPIG: before silencing the expression level of EDA+ fibronectin isoform was higher than the EDA- fibronectin, but as a result of silencing the amount of the two splice variants became comparable. In addition, the expression patterns of the splicing regulators were compared in two different synchronized, immortalized cell lines, HaCaT and HPV-KER cells. Gene and protein expression patterns of the three regulators were very similar in both cell lines during their proliferation and differentiation suggesting that they may share common regulation.

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