Related Experiment Video
Updated: Aug 18, 2026
Intratracheal Instillation of Stem Cells in Term Neonatal Rats
Published on: May 4, 2020
[A review on the effect of Claudin-18 on bronchopulmonary dysplasia in preterm infants]
Jing-Ye Zuo1, Ya-Jie Tong1, Dong-Mei Yue1
1Department of Neonatology, Shengjing Hospital, China Medical University, Shenyang 110004, China.
Insights
Bronchopulmonary dysplasia (BPD) involves lung barrier damage. Claudin-18 protein is crucial for lung development and may offer new BPD treatment strategies.
Area of Science:
- Pulmonary Medicine
- Cell Biology
- Developmental Biology
Background:
- Bronchopulmonary dysplasia (BPD) presents with early pulmonary edema and late alveolar obstruction/microvascular dysplasia.
- Lung epithelial barrier integrity is critical for preventing BPD pathogenesis.
- The Claudin family, particularly Claudin-18, regulates paracellular permeability and lung development.
Purpose of the Study:
- To investigate the role of Claudin-18 in the development and progression of Bronchopulmonary dysplasia (BPD).
- To explore Claudin-18's impact on lung epithelial permeability, alveolar development, and progenitor cell homeostasis.
- To identify potential new therapeutic targets for BPD.
Main Methods:
- Review of existing literature on Claudin-18 and BPD pathogenesis.
- Analysis of the function of Claudin-18 in lung epithelial barrier.
- Examination of Claudin-18 knockout models and their histopathological changes.
Main Results:
- Claudin-18 is the sole tight junction protein exclusively expressed in the lung.
- Lack of Claudin-18 leads to lung barrier dysfunction and impaired alveolar development.
- Claudin-18 knockout mice exhibit histopathological features consistent with BPD.
Conclusions:
- Claudin-18 plays a vital role in maintaining lung epithelial barrier function and normal alveolar development.
- Dysfunction of Claudin-18 is implicated in the pathogenesis of Bronchopulmonary dysplasia (BPD).
- Claudin-18 presents a promising target for novel BPD therapeutic strategies.
Abstract:
Bronchopulmonary dysplasia (BPD) has the main manifestations of pulmonary edema in the early stage and characteristic alveolar obstruction and microvascular dysplasia in the late stage, which may be caused by structural and functional destruction of the lung epithelial barrier. The Claudin family is the main component of tight junction and plays an important role in regulating the permeability of paracellular ions and solutes. Claudin-18 is the only known tight junction protein solely expressed in the lung. The lack of Claudin-18 can lead to barrier dysfunction and impaired alveolar development, and the knockout of Claudin-18 can cause characteristic histopathological changes of BPD. This article elaborates on the important role of Claudin-18 in the development and progression of BPD from the aspects of lung epithelial permeability, alveolar development, and progenitor cell homeostasis, so as to provide new ideas for the pathogenesis and clinical treatment of BPD.
