Abstract：
OBJECTIVE: To investigate the role of periostin (POSTN) and the transforming growth factor β (TGF-β) pathway in the formation of laryngotracheal stenosis (LTS) scar fibrosis and to explore the specific signaling mechanism of POSTN-regulated TGF-β pathway in tracheal fibroblasts.
METHODS: Bioinformatics analysis was performed on scar data sets from the GEO database to preliminarily analyze the involvement of POSTN and TGF-β pathways in fibrosis diseases. Expression of POSTN and TGF-β pathway-related molecules was analyzed in LTS scar tissue at the mRNA and protein levels. The effect of POSTN on the biological behavior of tracheal fibroblasts was studied using plasmid DNA overexpression and siRNA silencing techniques to regulate POSTN expression and observe the activation of TGF-β1 and the regulation of cell proliferation and migration via the TGF-β/RHOA pathway.
RESULTS: The bioinformatics analysis revealed that POSTN and the TGF-β pathway are significantly involved in fibrosis diseases. High expression of POSTN and TGF-β/RHOA pathway-related molecules (TGFβ1, RHOA, CTGF, and COL1) was observed in LTS tissue at both mRNA and protein levels. In tracheal fibroblasts, overexpression or silencing of POSTN led to the activation of TGF-β1 and regulation of cell proliferation and migration through the TGF-β/RHOA pathway.
CONCLUSIONS: POSTN is a key molecule in scar formation in LTS, and it regulates the TGF-β/RHOA pathway to mediate the formation of cicatricial LTS by acting on TGF-β1. This study provides insights into the molecular mechanisms underlying LTS and suggests potential therapeutic targets for the treatment of this condition.
METHODS: NA Laryngoscope, 134:4078-4087, 2024.
METHODS: Bioinformatics analysis was performed on scar data sets from the GEO database to preliminarily analyze the involvement of POSTN and TGF-β pathways in fibrosis diseases. Expression of POSTN and TGF-β pathway-related molecules was analyzed in LTS scar tissue at the mRNA and protein levels. The effect of POSTN on the biological behavior of tracheal fibroblasts was studied using plasmid DNA overexpression and siRNA silencing techniques to regulate POSTN expression and observe the activation of TGF-β1 and the regulation of cell proliferation and migration via the TGF-β/RHOA pathway.
RESULTS: The bioinformatics analysis revealed that POSTN and the TGF-β pathway are significantly involved in fibrosis diseases. High expression of POSTN and TGF-β/RHOA pathway-related molecules (TGFβ1, RHOA, CTGF, and COL1) was observed in LTS tissue at both mRNA and protein levels. In tracheal fibroblasts, overexpression or silencing of POSTN led to the activation of TGF-β1 and regulation of cell proliferation and migration through the TGF-β/RHOA pathway.
CONCLUSIONS: POSTN is a key molecule in scar formation in LTS, and it regulates the TGF-β/RHOA pathway to mediate the formation of cicatricial LTS by acting on TGF-β1. This study provides insights into the molecular mechanisms underlying LTS and suggests potential therapeutic targets for the treatment of this condition.
METHODS: NA Laryngoscope, 134:4078-4087, 2024.
摘要：
目的：研究骨膜素(POSTN)和转化生长因子β(TGF-β)通路在喉气管狭窄(LTS)瘢痕纤维化形成中的作用，探讨POSTN调控TGF-β通路在气管成纤维细胞中的特异性信号传导机制。
方法：对来自GEO数据库的瘢痕数据集进行生物信息学分析，以初步分析POSTN和TGF-β途径在纤维化疾病中的参与。在LTS瘢痕组织中从mRNA和蛋白水平分析POSTN和TGF-β途径相关分子的表达。采用质粒DNA过表达和siRNA沉默技术，研究POSTN对气管成纤维细胞生物学行为的影响，以调节POSTN的表达，观察TGF-β1的活化以及通过TGF-β/RHOA通路对细胞增殖和迁移的调控。
结果：生物信息学分析表明，POSTN和TGF-β途径与纤维化疾病密切相关。高表达POSTN和TGF-β/RHOA通路相关分子(TGF-β1,RHOA,CTGF,在LTS组织中观察到mRNA和蛋白质水平的COL1）。在气管成纤维细胞中，POSTN的过表达或沉默导致TGF-β1的激活以及通过TGF-β/RHOA途径调节细胞增殖和迁移。
结论：POSTN是LTS中瘢痕形成的关键分子，它调节TGF-β/RHOA通路，通过作用于TGF-β1介导瘢痕性LTS的形成。这项研究提供了对LTS潜在分子机制的见解，并提出了治疗这种疾病的潜在治疗目标。
方法：NA喉镜，2024.
方法：对来自GEO数据库的瘢痕数据集进行生物信息学分析，以初步分析POSTN和TGF-β途径在纤维化疾病中的参与。在LTS瘢痕组织中从mRNA和蛋白水平分析POSTN和TGF-β途径相关分子的表达。采用质粒DNA过表达和siRNA沉默技术，研究POSTN对气管成纤维细胞生物学行为的影响，以调节POSTN的表达，观察TGF-β1的活化以及通过TGF-β/RHOA通路对细胞增殖和迁移的调控。
结果：生物信息学分析表明，POSTN和TGF-β途径与纤维化疾病密切相关。高表达POSTN和TGF-β/RHOA通路相关分子(TGF-β1,RHOA,CTGF,在LTS组织中观察到mRNA和蛋白质水平的COL1）。在气管成纤维细胞中，POSTN的过表达或沉默导致TGF-β1的激活以及通过TGF-β/RHOA途径调节细胞增殖和迁移。
结论：POSTN是LTS中瘢痕形成的关键分子，它调节TGF-β/RHOA通路，通过作用于TGF-β1介导瘢痕性LTS的形成。这项研究提供了对LTS潜在分子机制的见解，并提出了治疗这种疾病的潜在治疗目标。
方法：NA喉镜，2024.
