肺泡上皮 paxillin 在出生后肺泡发育过程中的作用

IF 1.8 4区 生物学 Q3 BIOLOGY Biology Open Pub Date : 2025-02-24 DOI:10.1242/bio.061939
Mikaela Scheer, Priscilla Kyi, Tadanori Mammoto, Akiko Mammoto
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引用次数: 0

摘要

病灶粘附蛋白 paxillin 在胚胎发育过程中发挥着重要作用。我们曾报道 paxillin 控制细胞定向运动和血管生成。paxillin在肺部发育中的作用仍不清楚。与 P0(囊状期)相比,小鼠肺泡上皮 2 型(AT2)细胞在出生后第 10 天(肺泡期)的 Paxillin 表达更高。在他莫昔芬诱导的 PxniΔAT2 新生儿小鼠中,AT2 细胞中的 paxillin 水平被敲除,肺泡和血管结构被破坏,肺顺应性降低,出生后存活率降低。PxniΔAT2新生小鼠肺中的表面活性蛋白表达和片状体结构也受到抑制。在 PxniΔAT2 新生小鼠 AT2 细胞中,控制表面活性物质平衡的脂质转运体 ABCA3 及其转录调节因子 CEBPA 的表达受到抑制。这些发现表明,在AT2细胞中,paxillin通过CEBPA-ABCA3信号传导控制肺泡发育。调节AT2细胞中的paxillin可能是治疗新生儿肺发育障碍的新型干预措施。
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Alveolar epithelial paxillin in postnatal lung alveolar development.

Focal adhesion protein, paxillin plays an important role in embryonic development. We have reported that paxillin controls directional cell motility and angiogenesis. The role of paxillin in lung development remains unclear. Paxillin expression is higher in mouse pulmonary alveolar epithelial type 2 (AT2) cells at postnatal day (P)10 (alveolar stage) compared to P0 (saccular stage). The alveolar and vascular structures are disrupted, lung compliance is reduced, and the postnatal survival rate is lower in tamoxifen-induced PxniΔAT2 neonatal mice, in which the levels of paxillin in AT2 cells are knocked down. Surfactant protein expression and lamellar body structure are also inhibited in PxniΔAT2 neonatal mouse lungs. The expression of lipid transporter ABCA3 and its transcriptional regulator CEBPA that control surfactant homeostasis is inhibited in PxniΔAT2 neonatal mouse AT2 cells. These findings suggest that paxillin controls lung alveolar development through CEBPA-ABCA3 signaling in AT2 cells. Modulation of paxillin in AT2 cells may be novel interventions for neonatal lung developmental disorder.

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来源期刊
Biology Open
Biology Open BIOLOGY-
CiteScore
3.90
自引率
0.00%
发文量
162
审稿时长
8 weeks
期刊介绍: Biology Open (BiO) is an online Open Access journal that publishes peer-reviewed original research across all aspects of the biological sciences. BiO aims to provide rapid publication for scientifically sound observations and valid conclusions, without a requirement for perceived impact.
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