Figure 6.

Schematic of how thermal inkjet bioprinting triggers the activation of the VEGF pathway. Heat from the printing process causes cellular heat stress leading to various pathways in which extracellular heat-shock proteins play an angiogenic role. (a) The electric current heats a heating element producing a bubble that collapses causing the ejection of droplets containing cells. (b) VEGF-A binds VEGFR and either activates the AKT-eNOS-HSP90 pathway or promotes angiogenesis directly [72]. (c) HSP27 binds the TLR-3 activating the NF-κB pathway to produce VEGF and induce angiogenesis [64]. (d) Mitochondrial HSP60 binds the TLR-4 [68] leading to the activation of angiogenesis [63, 73]. (e) HSP70 binds TLR 2 and TLR-4 [71] leading to the activation of the NF-κB pathway to produce VEGF and induce angiogenesis [64, 74]. HSP = heat-shock protein, VEGFR = vascular endothelial growth factor receptor, eNOS = endothelial nitric oxide synthase, TLR = toll-like receptor, NF-κB = nuclear factor kappa-light-chain-enhancer of activated B cells.