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[侵袭性成纤维细胞中细胞凋亡的调控]

[Regulation of apoptosis in aggressive fibroblasts].

作者信息

Pap T

机构信息

Bereich Molekulare Medizin des Muskuloskeletalen Systems, Universitätsklinikum Münster, Domagkstrasse 3, 48149 Münster.

出版信息

Z Rheumatol. 2007 May;66(3):239-40, 242. doi: 10.1007/s00393-007-0167-3.

Abstract

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.

摘要

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。

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