通过ADAM10和在降粒过程中释放的蛋白酶,PrP从巨细胞的表面被切割出来
Steven D Willows1, Harissios Vliagoftis2, Valerie L Sim3,4
1Nanotechnology Research Centre, National Research Council Canada, 11421 Saskatchewan Dr, Edmonton, Alberta, T6G 2M9, Canada.
Journal of leukocyte biology
|May 10, 2024
概括
质蛋白通过ADAM10和蛋白酶从乳腺细胞排出,影响免疫细胞功能. 它的N端片段在喘患者中被检测到,这表明它在疾病中发挥了作用.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 神经科学是一个神经科学.
背景情况:
- 蛋白 (PrP) 的平稳功能仍在争论中.
- 蛋白在巨细胞上高度表达,这是炎症的关键调节者.
- 巨细胞激活导致PrP脱落,但机制和后果尚不清楚.
研究的目的:
- 为了研究瘤细胞中子蛋白的脱落机制.
- 为了确定蛋白对乳腺细胞活动的功能影响.
- 探索喘中蛋白碎片的临床相关性.
主要方法:
- 分析了对质蛋白表达和脱落的母细胞系.
- 用蛋白酶抑制剂和外源蛋白酶来研究蛋白分裂.
- 评估了ADAM10的依赖性.
- 使用prnp-/-巨细胞来评估功能变化.
- 在喘患者的体液中测量了蛋白片段.
主要成果:
- 乳腺细胞的质蛋白脱落是由ADAM10 (休息) 和乳腺细胞蛋白酶 (激活) 介导的.
- 巨细胞 (Prnp-/-) 中的蛋白缺乏导致降低脱粒化,细胞因子释放,以及降低FcεRI和CD117水平.
- 在人类唾液和血清中检测到一个N端的蛋白片段.
- 与对照组相比,喘患者的血清中这种片段减少了.
结论:
- 蛋白质通过不同的机制,根据细胞激活状态,从乳腺细胞中积极分裂.
- 蛋白在调节巨细胞功能方面发挥作用,影响脱粒和介质释放.
- 喘患者中N端蛋白片段的存在和水平的变化表明,喘患者可能在疾病发病过程中发挥作用.
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