Department of Dermatology, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Department of Dermatology, Kochi Medical School, Kochi University, Nankoku, Japan.
J Histochem Cytochem. 2018 Dec;66(12):847-862. doi: 10.1369/0022155418782693. Epub 2018 Jun 15.
Psoriasis is a complex chronic inflammatory skin disease characterized by epidermal thickening on the basis of increased keratinocyte proliferation and insufficient apoptosis. Laminins are important components of the basement membrane (BM) and impact on epidermal keratinocyte growth/apoptosis. Although several laminins are involved in the pathogenesis of psoriasis, it is still controversial about the expression patterns of laminin isoforms and which laminins are important in the development of psoriasis. Because laminin-511 and -332 are key BM components in human skin, and laminin-511 stimulates human hair follicle growth, we asked whether the BM zone in psoriasis shows any laminin-related abnormalities. This showed that the BM expression of laminin-511 and -332 was significantly increased within the skin lesion of psoriasis. Immunofluorescence microscopy revealed that laminin-511, -332, and collagen type IV proteins were also significantly increased in psoriasis-like skin lesions of Imiquimod-treated mice. Transmission electron microscopy showed a few gaps of lamina densa, and its thickness was significantly increased. Finally, laminin-511 treatment significantly stimulated the proliferation and inhibited apoptosis of HaCaT cells, while laminin-α5 chain gene knockdown decreased proliferation and induced apoptosis. These phenomenological observations raise the question of whether laminin-511-controlled keratinocyte growth/death may be a previously overlooked player in the pathogenesis of psoriatic epidermal lesions.
银屑病是一种复杂的慢性炎症性皮肤疾病,其特征是表皮在角质形成细胞增殖增加和凋亡不足的基础上增厚。层粘连蛋白是基底膜(BM)的重要组成部分,影响表皮角质形成细胞的生长/凋亡。尽管几种层粘连蛋白参与了银屑病的发病机制,但关于层粘连蛋白同工型的表达模式以及哪些层粘连蛋白在银屑病的发展中重要仍存在争议。由于层粘连蛋白-511 和 -332 是人类皮肤中关键的 BM 成分,并且层粘连蛋白-511 刺激人类毛囊生长,因此我们询问了银屑病中的 BM 区是否存在任何与层粘连蛋白相关的异常。结果表明,银屑病皮损中的层粘连蛋白-511 和 -332 的 BM 表达明显增加。免疫荧光显微镜显示,在咪喹莫特处理的小鼠类似银屑病的皮肤损伤中,层粘连蛋白-511、-332 和 IV 型胶原蛋白蛋白也明显增加。透射电子显微镜显示,致密层的几个间隙,其厚度明显增加。最后,层粘连蛋白-511 处理显著刺激了 HaCaT 细胞的增殖并抑制了其凋亡,而层粘连蛋白-α5 链基因敲低则减少了增殖并诱导了凋亡。这些现象学观察提出了一个问题,即层粘连蛋白-511 控制的角质形成细胞生长/死亡是否是银屑病表皮损伤发病机制中一个以前被忽视的因素。