Vascular endothelial growth factor (VEGF) inhibitors are targeted anti-cancer therapeutics with anti-angiogenic properties. Although effective against cell proliferation, these drugs can cause cardiotoxicity, including endothelial dysfunction. The effects of VEGF inhibitors on other vascular niche cells, particularly stem/stromal cells (MSCs) that are involved in vascular repair, remain unclear. Previously, we showed that extracellular vesicles (EVs) secreted from decidual mesenchymal stem cells (DMSCs) enhance endothelial cell proliferation. Therefore, we examined the effect of the VEGF inhibitor, sunitinib, on the DMSC growth profile, and the action of EVs derived from normal DMSCs, on sunitinib-treated DMSCs. EVs were isolated from DMSCs and characterized by nanoparticle tracking analysis and transmission electron microscopy. The xCELLigence system monitored the DMSC growth cycle over 144 hours. Various concentrations of sunitinib (2, 5, 7, 10, and 20 µM) were used to determine the half maximal inhibitory concentration (IC50). DMSC treatment was conducted using 7 µM sunitinib (IC50), with or without EVs at concentrations of 25, 50, and 100 µg/ml. Treatment with 7 μM sunitinib reduced DMSC proliferation by approximately 60%. Co-incubation with EVs at 50 and 100 μg/ml significantly enhanced proliferation, with the Cell Index increasing from 0.9 ± 0.1 (sunitinib alone) to 1.8 ± 0.1 at 48 hours (p < 0.05). These findings provide evidence that sunitinib reduces MSC proliferation in the vascular niche, but EVs can mitigate this effect and improve MSC growth. Treating patients with EVs may be a therapeutic strategy to alleviate the harmful effects of VEGF inhibitors by improving MSC function and repairing endothelial cell damage.