Myostatin-induced mechanisms of inflammatory bone and cartilage destruction by invasive fibroblast-like synoviocytes (A11*)

肌生长抑制素诱导的侵袭性成纤维样滑膜细胞炎症性骨和软骨破坏的机制 (A11*)

• 批准号: 320811199
• 金额: --
• 依托单位: Institut für Muskuloskelettale Medizin
• 依托单位国家: 德国
• 项目类别: Collaborative Research Centres
• 财政年份: 2016
• 资助国家: 德国
• 起止时间: 2015-12-31 至 2019-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/320811199?language=en
• 关键词: Myostatin; induced; mechanisms; inflammatory; bone

To investigate the role of myostatin in inflammatory destruction of tissue barriers, we will compare the effects of myostatin deficiency and phamacological inhibition on joint destruction in three arthritis models (different TNF-dependent). In addition, fibroblast-specific myostatin and activin wil be investigated by using Col1α2-Cre mice. Moreover, we want to evaluate the involvement of myostatin/ activin-mediated Smad2 signaling on synovial fibroblast-mediated matrix degradation by investigating proliferation, migration, apoptosis, invasive capacity, adhesion molecules, matrix-degrading proteases as well as involved signaling pathways.

为了研究肌生长抑制素在组织屏障炎症破坏中的作用，我们将比较肌生长抑制素缺乏和药理学抑制对三种关节炎模型（不同TNF依赖性）中关节破坏的影响。此外，将使用 Col1α2-Cre 小鼠研究成纤维细胞特异性肌生长抑制素和激活素。此外，我们希望通过研究增殖、迁移、凋亡、侵袭能力、粘附分子、基质降解蛋白酶以及所涉及的信号通路来评估肌生长抑制素/激活素介导的Smad2信号传导对滑膜成纤维细胞介导的基质降解的参与。