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TGF-α/EGFR信号传递促进了脂聚糖诱导的异常弹性质沉积和膜简化

Jianhui Li¹, Jian Cao², Chongbing Yan¹

¹Department of Neonatology, Shanghai Children's Hospital, School of Medicine, Shanghai Jiao Tong University, 355 Lu Ding Road, 200062, Shanghai, China.

Experimental cell research

|March 20, 2024

概括

在出生前暴露于炎症会增加支气管肺功能障碍 (BPD) 的风险,因为它会破坏弹性质. 通过EGFR抑制剂向转化生长因子-α (TGF-α) 信号,可以改善BPD的肺部发育.

科学领域:

肺部医学肺部医学
发展生物学发展生物学
细胞生物学细胞生物学

背景情况:

支气管肺功能障碍症 (BPD) 是早产婴儿的慢性肺部疾病,其特征是肺膜发育受损.
肺部异常的弹性质沉积是BPD的关键特征,阻碍了适当的气泡膜隔离和延伸.
产前炎症是BPD的重要危险因素,与异常的弹性质生产有关.

研究的目的:

研究转化生长因子-α (TGF-α) 信号在炎症诱导的异常弹性质沉积和BPD发展中的作用.
探索针对TGF-α/表皮生长因子受体 (EGFR) 途径在BPD的老鼠模型中的治疗潜力.

主要方法:

脂聚糖 (LPS) 用于诱导BPD在老鼠模型和人类肺上皮细胞 (BEAS-2B).
分析了TGF-α,lysyl氧化酶 (LOX) 和细胞分裂周期42 (Cdc42) 的表达水平.
一种EGFR抑制剂 (erlotinib) 对弹性质沉积和膜发育的影响在体内进行了评估.

主要成果:

通过托尔样受体4 (TLR4) /瘤坏死因子α转化酶 (TACE) 信号传导,LPS暴露显著上调TGF-α表达.
增加的TGF-α导致LOX过度激活和Cdc42在肌纤维细胞中的抑制,导致异常的弹性质沉积和受损的迁移.
埃洛提尼布治疗部分扭转了这些影响,改善了暴露于LPS的老鼠的弹性质沉积和膜结构.

结论:

在肺部发育过程中,TGF-α/EGFR信号传递在调节肌纤维细胞功能和弹性质沉积方面发挥着至关重要的作用.
这种途径的失调有助于在产前炎症后BPD的发病.
向TGF-α/EGFR通路代表了预防或治疗BPD的潜在治疗策略.

关键词:

支气管肺部发育不良症细胞分裂周期 42 细胞分裂周期 42 脂聚糖类糖化物脂聚糖类糖化物 Lysyl 氧化酶是一种溶解氧化剂.转化增长因子-α的转化增长因子

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