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Angiogenesis is a harmonized target for post-stroke recovery.Therefore, exploring the mechanisms involved in angiogenesis after stroke is vitally significant, but the epigenetic mechanisms behind endogenous angiogensis are still largely unknown.Over the past years, our research effort has been directed at post-stroke angiogenesis, and in this study we are reporting a miR-150 based mechanism underlying angiogenesis after stroke.We found that the decreased miR-150 expression in brain and serum of rats subjected to cerebral ischemia, and in oxygen-glucose deprived (OGD) brain microvascular endothelial cells (BMVECs) and astrocytes, is negatively related to cerebral angiogenesis after stroke.Up-regulation of miR-150 expression by intracerebro-ventricular injection of miR-150 agomir lead to decreased vascular density of infarct border zone (IBZ) and deteriorated functional recovery in permanent middle cerebral artery occlusion model (pMCAO) of rat.Furthermore, we found miR-150 decreased angiogenesis by direct regulation of expression of vascular endothelial growth factor (VEGF), which is therefore a direct target.In conclusion, our data suggested that miR-150 decreased post-stroke angiogenesis and recovery in rat through VEGF.It also potentiates the use of microRNAs as candidates for future epigenetic therapies in stroke treatment.