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博尔特佐米布通过减少人肺微血管内皮细胞中的细胞-细胞结合分子增加了血管透性

Taichi Matsumoto¹, Junichi Matsumoto², Yuka Matsushita³

¹Basic Medical Research Unit, St. Mary's Research Center, 422, Tsubuku-honmachi, Kurume 830-8543, Fukuoka, Japan.

International journal of molecular sciences

|July 14, 2023

概括

博尔特佐米布 (BTZ) 通过降低关键细胞-细胞结合蛋白的调节来增加肺血管透性. 这一发现揭示了多发性骨髓瘤患者BTZ诱导的肺毒性背后的机制.

科学领域:

肺血管生物学肺血管生物学
内皮细胞的功能是内皮细胞功能.
化疗引起的毒性化疗引起的毒性

背景情况:

博特佐米布 (Bortezomib,BTZ) 是一种用于多发性骨髓瘤的蛋白酶体抑制剂.
虽然BTZ可以引起严重的肺毒性,但其潜在机制尚未完全理解.
内皮膜屏障的完整性对肺部健康至关重要.

研究的目的:

调查BTZ对肺血管透性的影响.
检查BTZ对肺内皮细胞中细胞结节分子表达的影响.

主要方法:

使用人类肺微血管内皮细胞进行体外研究.
细胞单层透性的评估.
通过西班牙斑块和RT-qPCR对连接分子 (claudin-5,ocludin,ZO-1,VE-cadherin,β-catenin) 的蛋白质和mRNA表达的分析.

主要成果:

在临床相关度下,BTZ增加了肺微血管内皮细胞单层的透性.
BTZ显著降低了claudin-5,ocludin和VE-cadherin的蛋白质表达.
BTZ降低了克劳丁-5,奥克卢丁,ZO-1,VE-cadherin和β-catenin的mRNA表达.

结论:

通过降低关键细胞-细胞结合蛋白的调节,BTZ增强了肺血管的通透性.
克劳丁-5,奥克卢丁和VE-cadherin的下调似乎是BTZ诱导的肺毒性的关键机制.
这些发现为管理BTZ副作用提供了洞察力.

关键词:

粘附分子的粘附分子博尔特佐米布 (Bortezomib) 是一种药物.血管透性的血管透性

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