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The cerebral vasculature system plays an integral role in hypoxia\u2010induced cognitive defects by reducing oxygen and nutrition supply to the brain. RNA N6\u2010methyladenosine (m6A) is susceptible to modification and regulates gene expression in response to environmental changes, including hypoxia. However, the biological significance of m6A in endothelial cell performance under hypoxic conditions is unknown. Using m6A\u2010seq, RNA immunoprcipitation\u2010seq, and transcriptomic co\u2010analysis, the molecular mechanism of vascular system remodeling under acute hypoxia is investigated. A novel m6A reader protein, proline\u2010rich coiled\u2010coil 2B (PRRC2B), exists in endothelial cells. PRRC2B knockdown promoted hypoxia\u2010induced endothelial cell migration by regulating alternative splicing of the alpha 1 chain of collagen type XII in an m6A\u2010dependent manner and the decay of matrix metallopeptidase domain 14 and ADAM metallopeptidase domain 19 mRNA in an m6A\u2010independent manner. In addition, conditional knockout of PRRC2B in endothelial cells promotes hypoxia\u2010induced vascular remodeling and cerebral blood flow redistribution, thus alleviating hypoxia\u2010induced cognitive decline. Therefore, PRRC2B is integral in the hypoxia\u2010induced vascular remodeling process as a novel RNA\u2010binding protein. 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