Department of Dermatology and Allergology, University of Szeged, Hungary.
Arch Dermatol Res. 2011 Dec;303(10):745-52. doi: 10.1007/s00403-011-1162-8. Epub 2011 Jul 13.
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.
银屑病是一种慢性炎症性皮肤病，影响大约 2-4%的人口。我们最近描述了一种新的非编码 RNA，即应激诱导的银屑病易感 RNA 基因（PRINS），它在非病变银屑病表皮中过度表达，其表达可被多种应激因素诱导，如血清饥饿、接触抑制、紫外线（UV）-B 照射、病毒感染和 HaCaT 细胞的翻译抑制。在本工作中，我们旨在比较正常人类角质形成细胞（NHKs）和 HaCaT 细胞中应激和微生物诱导的 PRINS 表达。由于核因子-κB（NF-κB）参与细胞应激反应，我们试图探索 NF-κB 和 PRINS 介导的信号转导途径之间是否存在联系在 NHKs 和 HaCaT 细胞中。我们发现 PRINS 的表达在 HaCaT 细胞和 NHKs 中对各种应激信号和微生物剂的反应不同：在翻译抑制和 UV-B 处理后，PRINS 表达的相似诱导具有不同的时间过程，而在微生物剂处理后，PRINS 表达在 HaCaT 细胞中明显诱导，而在 NHKs 中我们无法检测到类似的变化。为了探索 HaCaT 细胞中已知的 NF-κB 异常是否与这种差异的 PRINS 表达有关，我们用小干扰 RNA（siRNA）沉默 HaCaT 细胞和 NHKs 中的 PRINS 基因表达，并在脂多糖（LPS）处理后监测 NF-κB 信号转导。沉默 PRINS 对 LPS 诱导的 HaCaT 细胞和 NHKs 中 NF-κB 活性均无影响。我们的结果表明，PRINS 可能独立于 NF-κB 信号通路影响角质形成细胞功能。
