The EDA+ fibronectin splicing variant is overexpressed in psoriatic non-lesional epidermis
and sensitizes keratinocytes to mitogenic signals. However, regulation of its abundance
is only partially understood. In our recent cDNA microarray experiment, we identified
three SR-rich splicing factors-splicing factor, arginine/serine-rich 18 (SFRS18),
peptidyl-prolyl cis-trans isomerase G (PPIG), and luc-7 like protein 3 (LUC7L3)-which
might be implicated in the preactivated states of keratinocytes in psoriatic non-involved
skin and could also contribute to the regulation of fibronectin mRNA maturation. In
this study, we investigated the role of LUC7L3, PPIG, and SFRS18 in psoriasis and
in the mRNA maturation process of fibronectin. Regarding tissue staining experiments,
we were able to demonstrate a characteristic distribution of the splicing factors
in healthy, psoriatic non-involved and involved epidermis. Moreover, the expression
profiles of these SR-rich proteins were found to be very similar in synchronized keratinocytes.
Contribution of splicing facwwtors to the EDA+ fibronectin formation was also confirmed:
their siRNA silencing leads to altered fibronectin mRNA and protein expression patterns,
suggesting the participation in the EDA domain inclusion. Our results indicate that
LUC7L3, PPIG, and SFRS18 are not only implicated in EDA+ fibronectin formation, but
also that they could possess multiple roles in psoriasis-associated molecular abnormalities.
