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Background  Neural precursor cell ( NPC ) migration toward lesions is key for neurological functional recovery. The neovasculature plays an important role in guiding  NPC  migration. Micro RNA ‐210 (miR‐210) promotes angiogenesis and neurogenesis in the subventricular zone and hippocampus after cerebral ischemia; however, whether miR‐210 regulates  NPC  migration and the underlying mechanism is still unclear. This study investigated the role of miR‐210 in  NPC  migration.    Methods and Results  Neovascularization and  NPC  accumulation was detected around ischemic foci in a mouse model of middle cerebral artery occlusion ( MCAO ) and reperfusion. Bone marrow–derived endothelial progenitor cells ( EPC s) were found to participate in neovascularization. miR‐210 was markedly upregulated after focal cerebral ischemia/reperfusion. Overexpressed miR‐210 enhanced neovascularization and  NPC  accumulation around the ischemic lesion and vice versa, strongly suggesting that miR‐210 might be involved in neovascularization and  NPC  accumulation after focal cerebral ischemia/reperfusion. In vitro experiments were conducted to explore the underlying mechanism. The transwell assay showed that  EPC s facilitated  NPC  migration, which was further promoted by miR‐210 overexpression in  EPC s. In addition, miR‐210 facilitated  VEGF ‐C (vascular endothelial growth factor C) expression both in vitro and in vivo. Moreover, the luciferase reporter assay demonstrated that miR‐210 directly targeted the 3′ untranslated region of SOCS1 (suppressor of cytokine signaling 1), and miR‐210 overexpression in  HEK 293 cells or  EPC s decreased  SOCS 1 and increased STAT3 (signal transducer and activator of transcription 3) and VEGF‐C expression. When  EPC s were simultaneously transfected with miR‐210 mimics and  SOCS 1, the expression of  STAT 3 and  VEGF ‐C was reversed.    Conclusions  miR‐210 promoted neovascularization and  NPC  migration via the  SOCS 1– STAT 3– VEGF ‐C pathway.

journal of the american heart association

Micro RNA ‐210 Promotes Accumulation of Neural Precursor Cells Around Ischemic Foci After Cerebral Ischemia by Regulating the SOCS1–STAT3–VEGF‐C Pathway