Medical Proteomics Research Center, KRIBB, Daejeon, Republic of Korea.
Int J Mol Med. 2011 Nov;28(5):785-92. doi: 10.3892/ijmm.2011.757. Epub 2011 Jul 25.
Psoriasis is a chronic inflammatory skin disease, characterized by a combination of abnormal proliferation of keratinocytes, immunology and vascular proliferation. Proteomic analyses have revealed some clues regarding the pathogenesis of psoriasis. In the present study, we conducted an investigation of different proteomes of psoriatic lesional skin, and compared them with those of normal and non-lesional psoriatic skin. We performed 2-D gel electrophoresis, liquid chromatography tandem mass spectrometry (LC-MS/MS) analysis and database searches. Expression of proteins were evaluated by immunoblot and immunohistochemistry analyses. Our data showed differential expression of 74 and 145 protein spots in non-lesional and lesional psoriatic skin, respectively. Eleven of 36 proteins, which were identified by LC-MS/MS, were categorized as apoptosis-regulating proteins. Other protein spots were categorized as proteins with involvement in the negative regulation of apoptosis, defense response-related proteins and inflammatory response. Of particular interest, increased expression of glutathione S transferase 1 (GSTP1) and peroxiredoxin 2 (PRDX2), which are involved in the Redox balance system, and SFN, which is involved in the cellular proliferation system, was observed in psoriatic lesional skin. Localization of GSTP1 and SFN was observed above the middle layer of the epidermis in psoriatic skin lesions. Expression of PRDX2 was clearly observed below the middle layer of the epidermis in chronic type psoriatic skin lesions. Taken together, 36 identified proteins were associated with biological regulation, including regulation of cell death, defense response, inflammatory response and reactive oxygen species (ROS) regulation. PRDX2 and GSTP1 may play roles in compensating mechanisms for reduction of ROS stress, and SFN may play roles in prevention of cancer development in proliferating cells through G2/M cell cycle arrest upon accidental DNA damage within psoriatic skin lesions.
银屑病是一种慢性炎症性皮肤病，其特征是角质形成细胞异常增殖、免疫学和血管增殖的结合。蛋白质组学分析为银屑病的发病机制提供了一些线索。在本研究中，我们对银屑病皮损的不同蛋白质组进行了研究，并将其与正常和非皮损银屑病皮肤进行了比较。我们进行了 2-DE 凝胶电泳、液相色谱串联质谱（LC-MS/MS）分析和数据库搜索。通过免疫印迹和免疫组织化学分析评估蛋白质的表达。我们的数据显示，非皮损和皮损银屑病皮肤中分别有 74 和 145 个蛋白斑点表达差异。通过 LC-MS/MS 鉴定的 36 种蛋白质中的 11 种被归类为凋亡调节蛋白。其他蛋白斑点被归类为参与负凋亡调节、防御反应相关蛋白和炎症反应的蛋白。特别值得注意的是，在银屑病皮损中观察到谷胱甘肽 S 转移酶 1（GSTP1）和过氧化物酶 2（PRDX2）的表达增加，它们参与了氧化还原平衡系统，而 SFN 则参与了细胞增殖系统。在银屑病皮损中，GSTP1 和 SFN 的定位在上皮中层以上，PRDX2 的表达在下皮中层以下。总之，36 种鉴定的蛋白质与生物调节有关，包括细胞死亡、防御反应、炎症反应和活性氧（ROS）调节的调节。PRDX2 和 GSTP1 可能在减少 ROS 应激的补偿机制中发挥作用，SFN 可能通过在银屑病皮损中的偶然 DNA 损伤时阻止 G2/M 细胞周期阻滞，在增殖细胞中预防癌症发展方面发挥作用。
