Skip to main content
. Author manuscript; available in PMC: 2020 May 22.
Published in final edited form as: Biofabrication. 2019 Jul 9;11(4):045005. doi: 10.1088/1758-5090/ab25f9

Figure 5.

Figure 5.

In vitro human phospho-kinase array analysis of the activation of 45 kinases in HMVECs after a 12 h incubation period. (a) STAT3, Fyn, TOR, AKT 1/2/3 were significantly overactivated among MP-HMVECs as compared to TIB-HMVECs.(b) Yes, CREB, Src, Chk-2, AMPKα1, c-JUN, FAK, GSK-3α/β, and JNK 1/2/3 were significantly overactivated among MP-HMVECs as compared to TIB-HIMVECs while HSP27 and HSP60 were overactivated significantly in TIB-HMVECs in comparison MP-HMVECs. STAT = signal transducer and activator of transcription proteins, EGF R = epidermal growth factor receptor, PDGF R = platelet-derived growth factor receptor, AKT = protein kinase B, PYK-2 = proline-rich tyrosine kinase 2, CREB = cAMP response element-binding protein, WNK1 = lysine deficient protein kinase 1, AMPK = adenosine monophosphate-activated protein kinase, eNOS = endothelial nitric oxide synthase, MSK = mitogen- and stress-activated protein kinase, GSK = glycogen synthase kinase, JNK = Jun N-terminal kinase, PRAS = proline-rich AKT substrate, HSP = heat-shock protein, TIB = thermal inkjet bioprinted, MP = manually pipetted, HMVECs = human microvascular endothelial cells. *P < 0.05; **P < 0.01; ***P < 0.001.