Pap T
Bereich Molekulare Medizin des Muskuloskeletalen Systems, Universitätsklinikum Münster, Domagkstrasse 3, 48149 Münster.
Z Rheumatol. 2007 May;66(3):239-40, 242. doi: 10.1007/s00393-007-0167-3.
Apoptosis is a central physiological mechanism for maintaining cellular stability in tissue. Synovial fibroblasts, which play a central role in the pathogenesis of rheumatoid arthritis (RA), show a resistance to apoptosis. Several molecular mechanisms are involved in such resistance. Thus, soluble Fas can bind Fas ligands (Fas-L) and hinder Fas-L induced apoptosis in fibroblasts. SUMO-1 (a small ubiquitin-like modifier) attaches to proteins post-translationally. This appears to be significantly involved in apoptosis resistance in RA fibroblasts. SUMO-1 levels are substantially increased in synovial fibroblasts from RA patients. A change in the post-translational SUMOlation pattern could represent a new target for changing the stable activation of synovial fibroblasts in RA.
细胞凋亡是维持组织中细胞稳定性的核心生理机制。在类风湿性关节炎（RA）发病机制中起核心作用的滑膜成纤维细胞表现出对细胞凋亡的抗性。这种抗性涉及多种分子机制。因此，可溶性Fas可结合Fas配体（Fas-L）并阻碍Fas-L诱导的成纤维细胞凋亡。SUMO-1（一种小泛素样修饰物）在翻译后附着于蛋白质。这似乎与RA成纤维细胞的凋亡抗性密切相关。RA患者滑膜成纤维细胞中SUMO-1水平显著升高。翻译后SUMO化模式的改变可能代表改变RA滑膜成纤维细胞稳定活化的新靶点。
