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通过调节MAPKs介导的气道光滑肌细胞功能障碍,LAPTM5增强了气道重塑的作用

Lijiao Jiang¹, Yaping Ying¹, Haihong Jin²

¹Department of Pediatrics, Taizhou Hospital of Zhejiang Province, No. 150 Ximen Street, Taizhou, 317000, Zhejiang Province, China.

Mammalian genome : official journal of the International Mammalian Genome Society

|February 16, 2026

概括

lysosome-associated protein transmembrane 5 (LAPTM5) 在喘气道光滑肌细胞 (ASMCs) 中进行上调. LAPTM5驱动ASMC的扩散和细胞外基质的产生,这表明它.

科学领域:

* 呼吸系统医学呼吸系统医学
* 细胞生物学 * 细胞生物学
* 免疫学免疫学

背景情况:

*呼吸道重塑是喘的一个关键特征,涉及呼吸道光滑肌肉细胞 (ASMC) 失调.
* Lysosome-associated protein transmembrane 5 (LAPTM5) 在喘病变发生过程中的特定作用尚不清楚.

研究的目的:

*研究喘患者的ASMC中LAPTM5的表达和功能.
* 探索LAPTM5在血小板衍生生长因子 (PDGF) 诱导的ASMC增殖,迁移和细胞外基质生产中的作用.
* 阐明基因激活蛋白激酶 (MAPK) 在LAPTM5-介导的ASMC失调中信号通路的参与.

主要方法:

*使用公开数据集对喘患者和非喘患者在ASMC中的LAPTM5表达的分析.
*体外实验涉及PDGF挑战,LAPTM5淘汰 (使用小干扰RNA) 和LAPTM5在ASMC中的过度表达.
*西部斑点分析检测MAPK信号通路激活 (-p38和-ERK).
* 用SB203580和U0126对MAPK进行药理抑制,以评估它们对ASMC功能的影响.

主要成果:

*LAPTM5在喘患者的ASMC中过度表达.
* PDGF诱导的ASMCs的增殖,迁移和细胞外矩阵生产被LAPTM5敲击抑制.
*LAPTM5过度表达增强了PDGF诱导的ASMC增殖,迁移和细胞外矩阵生产.
*LAPTM5 除减少了PDGF诱导的p38和ERK MAPKs的激活.
*MAPK抑制取消了LAPTM5过度表达引起的ASMC失调.

结论:

*LAPTM5表达与ASMC失调和喘中的呼吸道重塑显著相关.
*LAPTM5在通过MAPK信号传递调解PDGF诱导的ASMC反应方面发挥着关键作用.
*LAPTM5代表了管理喘和预防气道重塑的潜在治疗标.

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