Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 281, Issue 22, Pages 15554-15563Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M602003200
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- NHLBI NIH HHS [P01-HL65608, R01-HL53338] Funding Source: Medline
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Bone marrow-derived cells are recruited to sites of ischemia, where they promote tissue vascularization. This response is dependent upon the expression of vascular endothelial growth factor ( VEGF) receptor 1 ( VEGFR1), which mediates cell migration in response to VEGF or placental growth factor ( PLGF). In this study, we found that exposure of cultured mouse bone marrow-derived mesenchymal stromal cells ( MSC) to hypoxia or an adenovirus encoding a constitutively active form of hypoxia-inducible factor 1 ( HIF-1) induced VEGFR1 mRNA and protein expression and promoted ex vivo migration in response to VEGF or PLGF. MSCin which HIF-1 activity was inhibited by a dominant negative or RNA interference approach expressed markedly reduced levels of VEGFR1 and failed to migrate or activate AKT in response to VEGF or PLGF. Thus, loss-of-function and gain-of-function approaches demonstrated that HIF-1 activity is necessary and sufficient for basal and hypoxia-induced VEGFR1 expression in bone marrow-derived MSC.
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