在子中,WNT3a诱导外部门膜纤维化和功能障碍
Jagadeesh Thippeswamy1,2, Merlin Mamachan2,3, Jennifer Shin2
1Department of Medicine, Division of Gastroenterology, University of California, San Diego, CA.
在子中,Wnt3a诱导外部关节纤维化和功能障碍,降低门压力. 这表明WNT对抗剂可以治疗受伤或衰老引起的EAS功能障碍.
科学领域:
- 胃肠病学 胃肠病学
- 肌肉生理学 肌肉生理学
- 细胞信号传递 细胞信号传递
背景情况:
- 外关节 (EAS) 损伤和衰老导致纤维化和功能障碍,导致便失禁.
- WNT/β-catenin信号通路与各种组织的纤维化有关,包括骨肌肉.
研究的目的:
- 调查WNT激动剂Wnt3a是否会诱导EAS肌肉中的纤维化和功能障碍.
- 探索EAS功能障碍的潜在治疗点.
主要方法:
- 成年雌子接受了局部Wnt3a或盐水注射到EAS.
- 门通道的压力是通过力度计测量.
- EAS肌肉经历了组织学,免疫光,免疫组织化学 (IHC),西部斑块和蛋白质组分析.
主要成果:
- Wnt3a治疗显著降低了门通道压力,并减少了肌肉面积和纤维厚度.
- 组织学显示结缔组织增加,原沉积,以及β-catenin,TGF-β和Vimentin的水平升高.
- 蛋白质组学表明改变了参与肌肉收缩,纤维化和缩的途径.
结论:
- 直接使用WNT激动剂促进EAS纤维化和功能障碍,模仿与年龄有关的和受伤引起的变化.
- WNT对抗剂可能提供预防关节功能障碍的治疗策略.
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