ArticleScientific reports2026
miR-181a-5p of MSCs-derived exosomes promote vascular formation and cell proliferation by PTEN/PI3K/AKT axis in HUVECs.
Article in Scientific reports, 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
Our previous studies have demonstrated that exosomes play a crucial role in promoting vaginal tissue reconstruction in rats. The present study aims to elucidate the molecular mechanisms through which human umbilical cord mesenchymal stem cell-derived exosomes (hUMSC-Exos), which carry microRNA-181a-5p (miR-181a-5p), promote vascularization and tissue regeneration, with particular focus on the involvement of the PTEN/PI3K/AKT signaling pathway. Human umbilical vein endothelial cells (HUVECs) served as a model for studying angiogenesis and cell proliferation, and the expression levels of miR-181a-5p, PTEN, phospho-PI3K (p-PI3K), and phospho-AKT (p-AKT) were analyzed. HUVECs were transfected with PTEN overexpression vector or a negative control vector, then treated with exosomes derived from mesenchymal stem cells (MSCs) transfected with either a miR-181a-5p mimic or an inhibitor. Cell proliferation and migration were assessed using the Cell Counting Kit-8 and scratch assay, respectively, while cell invasion was evaluated via Transwell assay. The StarBase tool was employed to predict binding sites between miR-181a-5p and its target gene, the phosphatase and tensin homolog (PTEN). This interaction was subsequently validated using a dual-luciferase reporter assay. In HUVECs, elevated miR-181a-5p levels were positively correlate with reduced PTEN expression. In vitro experiments demonstrate that hUMSC-Exos enhance HUVEC migration, proliferation, and tube formation. Furthermore, overexpression of PTEN partially counteracted these miR-181a-5p-mediated effects. Our findings indicate that hUMSC-Exos contain miR-181a-5p, which may enhance tube formation and proliferation in HUVECs by regulating PTEN expression, thereby influencing the PI3K/AKT pathway.
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