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蛋白质组分析揭示了氧化酸化和JAK-STAT途径介导的原虫病变

Yuqi Cheng^1,2,3, Mingming Zhao^1,2,3, CaiHong Zhu^1,2,3

¹Department of Dermatology, The First Affiliated Hospital, Anhui Medical University, Hefei, Anhui, China.

Experimental dermatology

|October 7, 2024

概括

原虫 (PV) 的发病包括活性氧化酸化 (OXPHOS) 和JAK-STAT1通路. 抑制OXPHOS (甲福明) 和JAK1 (托法西提尼布) 的药物通过降低PV中的细胞分离来显示治疗潜力.

科学领域:

免疫皮肤学免疫皮肤学
分子生物学分子生物学
蛋白质组学是指蛋白质组学.

背景情况:

黄 (Pemphigus vulgaris,简称PV) 是一种罕见的自身免疫性水泡性疾病,其致病机制尚不清楚.
像LC-MS/MS这样的高通量蛋白质组技术对于通过分析皮肤蛋白质组来理解PV病原体至关重要.

研究的目的:

通过蛋白质组学分析,阐明Pemphigus vulgaris病变的潜在信号机制.
确定潜在的光伏疗法的关键途径和分子标.

主要方法:

蛋白质组分析 (LC-MS/MS) 和scRNA-seq在PV患者和健康对照的皮肤活检上.
在体外研究中,使用培养的角质细胞与PV血清治疗,随后进行免疫光和西部涂抹.
使用OXPHOS和JAK1抑制剂 (甲福林,托法西替尼) 的治疗效果的评估.

主要成果:

分别在病变与对照,非病变与对照和病变与非病变组中鉴定了880,605和586种差异表达蛋白 (DEP).
在PV中证明了氧化酸化 (OXPHOS) 途径的激活,在角质细胞中相关蛋白质的高表达.
在细胞模型中观察到OXPHOS蛋白,STAT1,p-STAT1和p-JAK1的表达增加;甲和托法西替尼都减弱了PV血清诱导的细胞分离.

结论:

这项研究表明,OXPHOS和JAK-STAT1信号通路在Pemphigus vulgaris的发病过程中起着重要作用.
甲胺和托法西提尼布通过向这些途径并减少角质细胞脱离,显示出治疗潜力.

关键词:

通过JAK-STAT1路径.在 LC-MS/MS 中使用.这是OXPHOS通道.

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