Eding Cecilia Bivik, Enerbäck Charlotta
Ingrid Asp Psoriasis Research Center, Department of Clinical and Experimental Medicine, Faculty of Medicine and Health Sciences, Linköping University, SE-581 85 Linköping, Sweden.
Acta Derm Venereol. 2017 Jul 6;97(7):788-796. doi: 10.2340/00015555-2656.
Psoriasis is a common autoimmune skin disease. The aim of this study was to investigate whether the apoptotic process is disturbed in psoriatic keratinocytes. In vitro culture of keratinocytes derived from both involved and uninvolved psoriatic skin, revealed higher viability and resistance to apoptosis following exposure to ultraviolet B, compared with cells from healthy controls. The position of apoptotic dysregulation was found to be upstream of cytochrome c release in the mitochondrial apoptotic pathway. Microarray transcriptome analysis revealed that 87 genes were differentially expressed in both involved and uninvolved psoriatic keratinocytes compared with controls. Among these, a general upregulation of anti-apoptotic genes and downregulation of pro-apoptotic genes were identified. This distinct apoptosis-resistant phenotype, unrelated to the inflammatory component of the disease, implies that intrinsic abnormalities in keratinocytes may contribute to the pathogenesis of psoriasis.
银屑病是一种常见的自身免疫性皮肤病。本研究的目的是调查银屑病角质形成细胞的凋亡过程是否受到干扰。对来自银屑病受累皮肤和未受累皮肤的角质形成细胞进行体外培养，结果显示，与健康对照细胞相比，暴露于紫外线B后，这些角质形成细胞具有更高的活力和抗凋亡能力。凋亡失调的位置被发现位于线粒体凋亡途径中细胞色素c释放的上游。微阵列转录组分析显示，与对照相比，在银屑病受累和未受累角质形成细胞中均有87个基因差异表达。其中，抗凋亡基因普遍上调，促凋亡基因下调。这种与疾病炎症成分无关的独特抗凋亡表型表明，角质形成细胞的内在异常可能有助于银屑病的发病机制。
