Journal
JOURNAL OF IMMUNOLOGY
Volume 171, Issue 5, Pages 2637-2643Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.171.5.2637
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Funding
- NHLBI NIH HHS [R01 HL063800, R01 HL067176, R01 HL 6108, P01 HL070294, R01 HL 63800, P01 HL 70294, R01 HL 67176] Funding Source: Medline
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The impact of the immune response in malignancy is poorly understood. While immune cells can destroy transformed cells, the targeting and accumulation of monocytes and macrophages at tumor sites may promote tumor metastases. The growth factor M-CSF is important in promoting monocyte survival. Since M-CSF-/- mice are protected against tumor metastases, we hypothesized that M-CSF induced monocytes to produce angiogenic factors that facilitate metastases. In this study we demonstrate that recombinant human M-CSF induces freshly isolated normal human monocytes to produce and release the growth factor vascular endothelial growth factor (VEGF) in a dose-dependent manner, which peaked at 5 days in culture. VEGF released by these monocytes is biologically active, as cell-free supernatants from these M-CSF-stimulated monocytes induced tube formation,in HUVEC. Network formation by these HUVECs after treatment with supernatants from monocytes stimulated with M-CSF were inhibited by anti-VEGF, but not by the isogenic control, Abs. Collectively, these data support an important role for M-CSF and monocytes in VEGF production and angiogenesis.
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