Correlation Engine 2.0
Clear Search sequence regions


  • apoptosis (3)
  • bronchopulmonary dysplasia (11)
  • cellular (1)
  • claudin 1 (7)
  • humans (1)
  • hyperoxia (4)
  • lipid (5)
  • lung (2)
  • newborn (1)
  • pathogenesis (2)
  • pc 16 (8)
  • protect (1)
  • protein rat (1)
  • rat (3)
  • research (1)
  • rna (1)
  • SPC (1)
  • Sizes of these terms reflect their relevance to your search.

    Bronchopulmonary dysplasia (BPD) remains a significant challenge in neonatal care, the pathogenesis of which potentially involves altered lipid metabolism. Given the critical role of lipids in lung development and the injury response, we hypothesized that specific lipid species could serve as therapeutic agents in BPD. This study aimed to investigate the role of the lipid Phosphatidylcholine (PC) (16:0/14:0) in modulating BPD pathology and to elucidate its underlying mechanisms of action. Our approach integrated in vitro and in vivo methodologies to assess the effects of PC (16:0/14:0) on the histopathology, cellular proliferation, apoptosis, and molecular markers in lung tissue. In a hyperoxia-induced BPD rat model, we observed a reduction in alveolar number and an enlargement in alveolar size, which were ameliorated by PC (16:0/14:0) treatment. Correspondingly, in BPD cell models, PC (16:0/14:0) intervention led to increased cell viability, enhanced proliferation, reduced apoptosis, and elevated surfactant protein C (SPC) expression. RNA sequencing revealed significant gene expression differences between BPD and PC (16:0/14:0) treated groups, with a particular focus on Cldn1 (encoding claudin 1), which was significantly enriched in our analysis. Our findings suggest that PC (16:0/14:0) might protect against hyperoxia-induced alveolar type II cell damage by upregulating CLDN1 expression, potentially serving as a novel therapeutic target for BPD. This study not only advances our understanding of the role of lipids in BPD pathogenesis, but also highlights the significance of PC (16:0/14:0) in the prevention and treatment of BPD, offering new avenues for future research and therapeutic development. Copyright © 2024 Elsevier Ltd. All rights reserved.

    Citation

    Weiwei Hou, Boshi Yu, Yubai Li, Xudong Yan, Qian Su, Xiaoyan Fang, Xiaoguang Zhou, Zhangbin Yu. PC (16:0/14:0) ameliorates hyperoxia-induced bronchopulmonary dysplasia by upregulating claudin-1 and promoting alveolar type II cell repair. The international journal of biochemistry & cell biology. 2024 Jul;172:106587

    Expand section icon Mesh Tags

    Expand section icon Substances


    PMID: 38740281

    View Full Text