Transcriptional activation of hypoxia-inducible factor-1 (HIF-1) in myeloid cells promotes angiogenesis through VEGF and S100A8

• DOI: 10.1073/pnas.1320243111
• Publication Date: 2014-02-05T05:08:01Z
• Authors: G-One Ahn; Jun Seita; Beom-Ju Hong; Young-Eun Kim; Seoyeon Bok; Chan-Ju Lee; Kwang Soon Kim; Jerry C. Lee; Nicholas J. Leeper; John P. Cooke; Hak Jae Kim; Il Han Kim; Irving L. Weissman; J. Martin Brown
• Keywords: EXPRESSION; 0301 basic medicine; Blotting, Western; Neovascularization, Physiologic; HIF-1-ALPHA; Enzyme-Linked Immunosorbent Assay; Mice, Transgenic; THERAPY; Polymerase Chain Reaction; DISEASE; TUMOR ANGIOGENESIS; Mice; 03 medical and health sciences; Ischemia; Animals; Calgranulin A; Myeloid Cells; MACROPHAGES; Crosses, Genetic; DNA Primers; Analysis of Variance; INDUCTION; Flow Cytometry; CANCER; Hindlimb; 3. Good health; Drug Combinations; LEADS; ENDOTHELIAL GROWTH-FACTOR; Proteoglycans; Collagen; Hypoxia-Inducible Factor 1; Laminin

SignificanceHere, we are reporting our findings that hypoxia-inducible factor 1 (HIF-1) activation in monocytes promotes neovascularization in matrigel and improves blood flow in hindlimb ischemia through production of vascular endothelial growth factor and S100A8. We found that HIF-1 regulates S100A8 expression specifically in monocytes isolated from our unique strain of transgenic mice targeting HIF pathways.