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通过瘤内皮标记1调节矩阵重新加载,可以防止腹腔大动脉动脉瘤
Yi-Kai Hong1,2,3, Tsung-Lin Cheng4,5,6,7, Chao-Kai Hsu2,3,8
1Department of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
International journal of biological sciences
|August 8, 2024
概括
瘤内皮标记物1 (TEM1) 调节血管细胞中的原合成,影响腹腔大动脉瘤 (AAA) 的形成. 使用TEM1恢复矩阵完整性可能为AAA提供治疗策略.
科学领域:
- 血管生物学 血管生物学
- 矩阵生物学 矩阵生物学
- 再生医学是一种再生医学.
背景情况:
- 腹腔大动脉瘤 (AAA) 是一种危及生命的疾病,涉及血管炎症和矩阵退化.
- 瘤内皮标记1 (TEM1) 与组织重塑和修复有关.
- 人类AAA中TEM1表达升高,源自血管光滑肌细胞 (VSMC) 和纤维细胞.
研究的目的:
- 调查TEM1在AAA病变发生过程中的作用.
- 在AAA中探索TEM1的治疗潜力.
主要方法:
- 对人类AAA组织和CaCl2诱导的小鼠AAA模型的分析.
- 在VSMC和纤维细胞中进行TEM1静音化和重组TEM1 (rTEM1) 管理.
- 对基因表达 (COL1A1),蛋白质酸化 (SMAD2),原蛋白含量和弹性质完整性的评估.
主要成果:
- 在AAA中增加TEM1表达与原基因表达和含量相关.
- 抑制TEM1抑制了TGF-β1诱导的VSMC/纤维细胞变化和原合成,在小鼠中加剧了AAA.
- 在小鼠模型中,rTEM1促进了VSMC/纤维细胞表型变化,原合成,并减弱了AAA发育.
结论:
- 居住在树皮细胞中的TEM1调节了原合成,抵消了AAA中的大动脉壁衰竭.
- rTEM1治疗增强了矩阵完整性,并显示了AAA的治疗潜力.
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