Overexpression of FoxM1 Enhanced the Protective Effect of Bone Marrow-Derived Mesenchymal Stem Cells on Lipopolysaccharide-Induced Acute Lung Injury through the Activation of Wnt/ β-Catenin Signaling

Oxid Med Cell Longev. 2023 Feb 11:2023:8324504. doi: 10.1155/2023/8324504. eCollection 2023.

Abstract

Background: Mesenchymal stem cell- (MSC-) based cell and gene therapies have made remarkable progress in alleviating acute lung injury/acute respiratory distress syndrome (ALI/ARDS). However, the benefits of Forkhead box protein M1 (FoxM1) gene-modified MSCs in the treatment of ALI have not been studied.

Methods: We evaluated the therapeutic effects of FoxM1-modified MSCs in ALI mice induced by lipopolysaccharide (LPS) by quantifying the survival rate, lung weight ratio (wet/dry), and contents of bronchoalveolar lavage fluid. In addition, microcomputed tomography, histopathology, Evans Blue assay, and quantification of apoptosis were performed. We also explored the underlying mechanism by assessing Wnt/β-catenin signaling following the treatment of mice with FoxM1-modified MSCs utilizing the Wnt/β-catenin inhibitor XAV-939.

Results: Compared with unmodified MSCs, transplantation of FoxM1-modified MSCs improved survival and vascular permeability; reduced total cell counts, leukocyte counts, total protein concentrations, and inflammatory cytokines in BALF; attenuated lung pathological impairments and fibrosis; and inhibited apoptosis in LPS-induced ALI/ARDS mice. Furthermore, FoxM1-modified MSCs maintained vascular integrity during ALI/ARDS by upregulating Wnt/β-catenin signaling, which was partly reversed via a pathway inhibitor.

Conclusion: Overexpression of FoxM1 optimizes the treatment action of MSCs on ALI/ARDS by inhibiting inflammation and apoptosis and restoring vascular integrity partially through Wnt/β-catenin signaling pathway stimulation.

MeSH terms

  • Acute Lung Injury* / chemically induced
  • Animals
  • Bone Marrow / metabolism
  • Lipopolysaccharides / pharmacology
  • Lung / pathology
  • Mesenchymal Stem Cell Transplantation*
  • Mesenchymal Stem Cells* / metabolism
  • Mice
  • Respiratory Distress Syndrome* / metabolism
  • Wnt Signaling Pathway
  • X-Ray Microtomography
  • beta Catenin / metabolism

Substances

  • beta Catenin
  • Lipopolysaccharides
  • Foxm1 protein, mouse