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抑制MRTF-A/SRF信号轴可以缓解声道的痕

Ryan M Friedman¹, Huy D Truong¹, Matthew R Aronson¹

¹Department of Bioengineering, School of Engineering and Applied Sciences, University of Pennsylvania, Philadelphia, PA 19104, USA; Division of Otolaryngology, Department of Surgery, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA.

Matrix biology : journal of the International Society for Matrix Biology

|February 16, 2025

概括

声的痕涉及纤维细胞到肌纤维细胞的过渡. 抑制MRTF-A (肌肉激素相关的转录因子A) 通过阻断这种途径来减少痕,提供了一个潜在的治疗标.

科学领域:

细胞生物学细胞生物学
耳鼻喉科耳鼻喉科耳鼻喉科
生物医学工程生物医学工程

背景情况:

声的痕,一个常见的原因声损伤后的损伤,源于纤维细胞到肌纤维细胞的转化.
肌纤维细胞的特征是细胞外基质 (ECM) 分泌量增加和应力纤维形成.
已知转化生长因子β1 (TGF-β1) 和矩阵刚性是这种转变的诱导因素.

研究的目的:

确定调节声中纤维细胞到肌纤维细胞激活的关键细胞内通路.
研究MRTF-A/SRF通路在声肌纤维细胞激活中的作用.
评估MRTF-A抑制的治疗潜力,在声音痕的小鼠模型中.

主要方法:

用TGF-β1.1.治疗的人类声纤维细胞的散装RNA测序.
在TGF-β1刺激和ECM硬化下对MRTF-A和SRF核转位的评估.
使用CCG-257,081进行MRTF-A的体外抑制,以评估对亲纤维细胞标记物和收缩性的影响.
评估MRTF-A抑制的声音痕的小鼠模型,分析组织学和分子变化.

主要成果:

在TGF-β1诱导的肌纤维细胞中,MRTF-A/SRF下游的基因被上调.
TGF-β1和ECM硬化促进了MRTF-A和SRF的核转移.
在实验室中,MRTF-A抑制减少了亲纤维细胞基因表达,α-SMA阳性细胞和纤维细胞收缩性.
在小鼠中,MRTF-A抑制降低了声音的痕严重程度,包括减少了上皮质加厚,糖氨基甘氨酸,原沉积和ACTA2表达.

结论:

该MRTF-A/SRF通路是声肌纤维细胞激活的关键调节器.
在小鼠模型中,MRTF-A的抑制显示出对声音痕的保护作用.
准MRTF-A/SRF通路代表了管理声痕的有希望的治疗策略.

关键词:

纤维母细胞细胞是如何形成的纤维化纤维化纤维化肌纤维母细胞细胞.上空气道上空气道上空气道.声带声带的声音.伤口愈合伤口愈合

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