ArticleThe journal of gene medicine2026
Bone Marrow Stem Cell Exosomes Protect Lung Cells from Oxygen Damage by Regulating miR-23a-3p/Slc7a2 Pathway.
Article in The journal of gene medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveMesenchymal stem cell exosomes (MSC-Exos) play crucial regulatory roles in the processes of alveolar epithelial cell development, proliferation, apoptosis and differentiation. The aim of this project was to explore the regulatory mechanism of the miR-23a-3p/Slc7a2 axis mediated by bone marrow MSC-derived exosomes in hyperoxia-induced injury to alveolar epithelial type II cells (AECIIs) in neonatal rats.
methodsThe miRBase and TargetScan databases were used to intersect and validate the differential expressions of microRNAs derived from BMSC exosomes in AECIIs under hyperoxic conditions and their target genes to construct in vitro and in vivo models of lung epithelial cell injury under hyperoxic conditions and to transfect BMSC-Exos. Dual-luciferase reporter assays were used to verify the binding relationship between miR-23a-3p and Slc7a2 and overexpression and siRNA plasmids for miR-23a-3p and Slc7a2 were constructed.
resultsmiR-23a-3p derived from BMSC exosomes directly targets Slc7a2 mRNA. miR-23a-3p antagonizes hyperoxia-induced apoptosis of AECIIs and promotes cell proliferation in vitro by inhibiting Slc7a2 expression (p < 0.05). miR-23a-3p inhibited, while Slc7a2 promoted, the expression of ROS in AECIIs. miR-23a-3p significantly ameliorated hyperoxia-induced lung tissue injury in neonatal rats and significantly reduced hyperoxia-induced apoptosis in neonatal rat lung tissue (p < 0.05). The miR-23a-3p/Slc7a2 axis significantly regulates the expression of multiple biochemical markers in the supernatant of AECIIs and in the serum of neonatal rats under hyperoxia conditions.
conclusionmiR-23a-3p derived from BMSC exosomes participates in the repair of lung epithelial cell injury under hyperoxic conditions by regulating the expression of its target gene Slc7a2.
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