title: Comparison of stress-induced PRINS gene expression in normal human keratinocytes and HaCaT cells.
abstract: Psoriasis is a chronic inflammatory skin disease that affects approximately 2-4% of the population. We recently described a novel non-coding RNA, psoriasis susceptibility related RNA gene induced by stress (PRINS), that was overexpressed in non-lesional psoriatic epidermis, and its expression was induced by various stress factors such as serum starvation, contact inhibition, ultraviolet (UV)-B irradiation, viral infection and translational inhibition in HaCaT cells. In the present work we set out to compare the stress and microbial agent-induced PRINS expression in normal human keratinocytes (NHKs) and HaCaT cells. Since nuclear factor-κB (NF-κB) is involved in the cellular stress response, we sought to explore whether there is a connection between the NF-κB and PRINS-mediated signal transduction pathways in NHKs and HaCaT cells. We found that the PRINS expression responded differentially to various stress signals and microbial agents in HaCaT cells and in NHKs: after translational inhibition and UV-B treatment, similar induction of PRINS expression occurred with different time courses while after microbial agent treatment, the PRINS expression was significantly induced in HaCaT cells, whereas we could not detect similar changes in NHKs. To explore whether the known NF-κB abnormalities in HaCaT cells could be related to this differential PRINS expression, we silenced the PRINS gene expression with small interfering RNA (siRNA) in both HaCaT cells and in NHKs and monitored NF-κB signal transduction after lipopolysaccharide (LPS) treatment. Silencing of PRINS had no effect on LPS-induced NF-κB activity either in HaCaT cells or in NHKs. Our results indicate that PRINS probably affects keratinocytes functions independently of NF-κB signalling.
authors.affiliation: Department of Dermatology and Allergology, University of Szeged, Hungary. barililla@hotmail.com
authors.forename: Lilla
authors.initials: L
authors.lastname: Bari
authors.forename: Sarolta
authors.initials: S
authors.lastname: Bacsa
authors.forename: Eniko
authors.initials: E
authors.lastname: Sonkoly
authors.forename: Zsuzsanna
authors.initials: Z
authors.lastname: Bata-Csörgo
authors.forename: Lajos
authors.initials: L
authors.lastname: Kemény
authors.forename: Attila
authors.initials: A
authors.lastname: Dobozy
authors.forename: Márta
authors.initials: M
authors.lastname: Széll
mesh_terms: D000942:Antigens, Bacterial / Q000378:metabolism; D002460:Cell Line; D003513:Cycloheximide / Q000494:pharmacology; D005786:Gene Expression Regulation / Q000187:drug effects / Q000235:genetics / Q000528:radiation effects; D006801:Humans; D015603:Keratinocytes / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology / Q000528:radiation effects; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D014176:Protein Biosynthesis / Q000187:drug effects; D011565:Psoriasis / Q000235:genetics / Q000378:metabolism*; D034741:RNA, Small Interfering / Q000235:genetics; D022661:RNA, Untranslated / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects / Q000235:genetics / Q000528:radiation effects; D013312:Stress, Physiological / Q000187:drug effects / Q000235:genetics / Q000528:radiation effects; D014466:Ultraviolet Rays / Q000009:adverse effects
chemical_list: D000942:Antigens, Bacterial; D016328:NF-kappa B; D034741:RNA, Small Interfering; D022661:RNA, Untranslated; D003513:Cycloheximide