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HIF1α plays stimulatory roles in the revascularization in ischemic area of cerebral ischemia.However,the hydroxylation of proline at 564 and asparagine at 803 in the HIF1α coding sequence(CDS)facilitated the degradation of HIF1α and inhibited the transcription activity of HIF1α promoter under normoxic conditions and confined the pro-angiogenic efficacy of HIF1α.In this study,HIF 1α mutant containing P564A and N803A was constructed by site-directed mutagenesis.Rat bone marrow mesenchymal stem cells(BMSCs)were infected with adenoviral particles containing HIF1α mutant at multiplicity of infection(MOI)of 150.