Figure 3.

Proposed model for the mechanistic function of MK in regulating vascular endothelial cell proliferation in arteriogenesis. During recruitment, leukocytes get in close contact with the endothelial cell surface, which is covered with CXCL-1, MCP-1 and MK. Upon integrin β₂ activation, VEGF-A is increased, expressed, and released from leukocytes. However, not only MK stored on endothelial cell surface, but also MK stored in leukocytes might contribute to increased bioavailability of VEGF-A. Upon binding to VEGFR2, VEGF-A promotes the expression of eNOS and nNOS relevant for endothelial cell proliferation. Adapted from Lautz et al., 2018 [76].