Journal
CYTOKINE
Volume 143, Issue -, Pages -Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.cyto.2021.155519
Keywords
Interferon-beta; Neuropilin-1; Vascular Endothelial Growth Factor; Monocytes; CD14; Chemotaxis
Funding
- NIH [R01 AI I100129, T32 AA013034]
- Judith Van Kampen Scholarship
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The study demonstrates that IFN-beta inhibits monocyte chemotaxis towards VEGF by downregulating NRP-1 expression, suggesting a mechanism by which type I interferons suppress angiogenesis by targeting circulating monocytes.
Type I interferons (IFNs) inhibit angiogenesis, the sprouting of new blood vessels, during tissue development, remodeling, and tumor growth. One of the major targets type I IFNs inhibit are circulating monocytes, which promote vascular development by secreting growth factors, chemokines, and proteases. This study tested the hypothesis that IFN-beta directly inhibits monocyte chemotaxis towards VEGF. We were interested in looking at chemotaxis towards VEGF because VEGF is known to create a pro-angiogenesis environment by acting as a stimulator and chemotactic factor for endothelial cells and monocytes. Here, we demonstrate that IFN-beta, a type I IFN, downregulates neuropilin-1 (NRP-1) expression by human monocytes and inhibits chemotaxis induced by vascular endothelial growth factor (VEGF), a NRP-1 ligand. Together, the data suggest that IFN-beta directly downregulates NRP-1 expression in monocytes, thus inhibiting monocyte chemotaxis toward a VEGF enriched environment.
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