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Overexpression of Wnt5a promoted the protective effect of mesenchymal stem cells on Lipopolysaccharide-induced endothelial cell injury via activating PI3K/AKT signaling pathway
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Overexpression of Wnt5a promoted the protective effect of mesenchymal stem cells on Lipopolysaccharide-induced endothelial cell injury via activating PI3K/AKT signaling pathway
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Overexpression of Wnt5a promoted the protective effect of mesenchymal stem cells on Lipopolysaccharide-induced endothelial cell injury via activating PI3K/AKT signaling pathway
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Journal Article
Overexpression of Wnt5a promoted the protective effect of mesenchymal stem cells on Lipopolysaccharide-induced endothelial cell injury via activating PI3K/AKT signaling pathway
2024
Overview
Background
Lung endothelial barrier injury plays an important role in the pathophysiology of acute lung injury/acute respiratory distress syndrome (ALI/ARDS). Mesenchymal stem cells (MSCs) therapy has shown promise in ARDS treatment and restoration of the impaired barrier function. It has been reported that Wnt5a shows protective effects on endothelial cells. Therefore, the study aimed to investigate whether overexpression of Wnt5a could promote the protective effects of MSCs on Lipopolysaccharide (LPS)-induced endothelial cell injury.
Methods
To evaluate the protective effects of MSCs overexpressing Wnt5a, we assessed the migration, proliferation, apoptosis, and angiogenic ability of endothelial cells. We assessed the transcription of protective cellular factors using qPCR and determined the molecular mechanism using Western blot analysis.
Results
Overexpression of Wnt5a upregulated the transcription of protective cellular factors in MSCs. Co-culture of MSC
Wnt5a
promoted endothelial migration, proliferation and angiogenesis, and inhibited endothelial cell apoptosis through the PI3K/AKT pathway.
Conclusions
Overexpression of Wnt5a promoted the therapeutic effect of MSCs on endothelial cell injury through the PI3K/AKT signaling. Our study provides a novel approach for utilizing genetically modified MSCs in the transplantation therapy for ARDS.
Publisher
BioMed Central,BioMed Central Ltd,Springer Nature B.V,BMC
Subject
1-Phosphatidylinositol 3-kinase
/ Acute respiratory distress syndrome
/ Analysis
/ Ethylenediaminetetraacetic acid
/ Genetically modified organisms
/ Humans
/ Injuries
/ Lipopolysaccharides - metabolism
/ Lungs
/ Medicine
/ Mesenchymal Stem Cells - metabolism
/ Phosphatidylinositol 3-Kinases - metabolism
/ Plasmids
/ Proto-Oncogene Proteins c-akt - metabolism
/ Respiratory distress syndrome
/ Respiratory Distress Syndrome - therapy
/ Wnt5a
