AI Article Synopsis
- Bone marrow-derived cells help promote blood vessel formation at sites of reduced blood flow (ischemia) by responding to signals like vascular endothelial growth factor (VEGF).
- This study showed that hypoxia or an active form of hypoxia-inducible factor 1 (HIF-1) increases the levels of VEGF receptor 1 (VEGFR1) in mouse bone marrow-derived mesenchymal stromal cells (MSC).
- Inhibiting HIF-1 reduced VEGFR1 levels and impaired the cells' ability to migrate and activate key signaling pathways in response to VEGF or placental growth factor (PLGF).
Article Abstract
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. MSC in 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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| http://dx.doi.org/10.1074/jbc.M602003200 | DOI Listing |
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