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柔滑肌肉特异性表达的基醇甲基转移酶减少了动脉损伤引起的内脏增生

Wei-Cheng Jiang¹, Chung-Huang Chen², Hua-Hui Ho²

¹Institute of Anatomy and Cell Biology, College of Medicine, National Yang Ming Chiao Tung University, Taipei, 112304, Taiwan.

Journal of biomedical science

|August 21, 2025

概括

在血管平滑肌细胞中,基转移酶 (HIOMT) 改变了酸的代谢,增加了保护性5-甲基酸 (5-MTP),降低了有害的血清素. 这种机制减轻了血管损伤和内脏增生.

科学领域:

生物化学和分子生物学
血管生物学
代谢调节

背景情况:

基因醇O-甲基转移酶 (HIOMT) 对于氨酸的合成至关重要,并且在非细胞中表达.
人类HIOMT (hHIOMT) 异型在各种细胞类型中表现出差异性活性,其中hHIOMT298在纤维细胞中活跃.
之前的研究表明外源的5-甲基三胺 (5-MTP) 能保护动脉,但其在血管光滑肌细胞 (VSMC) 中的内源合成尚不清楚.

研究的目的:

研究hHIOMT异型在VSMC中的作用和功能.
确定VSMC是否可以合成5-MTP及其对血管反应的影响.
阐明HIOMT影响血管损伤和炎症的分子机制.

主要方法:

用不同的hHIOMT异型感染初级VSMC并用炎症性细胞因子治疗以评估p38 MAPK激活.
通过动脉损伤模型生成全球和VSMC特定的hHIOMT转基因小鼠.
组织学分析,测量酸代谢物和酶,以及对芳香L-氨基酸脱酶 (AADC) 和血清素途径的操纵.

主要成果:

在转基因小鼠中,hHIOMT373的过度表达减弱了细胞因子诱导的p38 MAPK激活,并减少了内膜增生.
转基因动脉显示血清和AADC水平降低;IL- 1β治疗增加了VSMC中的AADC和血清,而5- MTP或HIOMT可以逆转这种情况.
血清激素通过ERK1/ 2促进VSMC增殖并降低VSMC标记物,而AADC操纵则影响VSMC标记物和增殖物.

结论:

在VSMC中,hHIOMT373重新编程了三甲的代谢,增加了5-MTP并降低了血清素,从而防止受伤引起的内膜增生.
通过抑制p38 MAPK激活,HIOMT-5-MTP途径抑制了AADC- serotonin的诱导,这表明它在血管疾病中起到了新的作用.
通过调节三甲代谢,HIOMT代表了血管疾病的潜在治疗标.

关键词:

五甲基三位基醇O-甲基转移酶在体内增生血清素血管平滑肌细胞

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