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. Author manuscript; available in PMC: 2020 Dec 5.
Published in final edited form as: Br J Haematol. 2020 Apr 28;190(4):599–609. doi: 10.1111/bjh.16671

Fig 6.

Fig 6.

Sickle RBC adhesion to heme-activated endothelial cells under physiologic hypoxia in microfluidic channels in vitro. Representative images of adherent RBCs to heme-activated endothelial cells are also shown in the control group (A, B on HUVECs and HPMECs) and in the imatinib-treated group (C, D on HUVECs and HPMECs). Arrows indicate RBCs adherent to endothelium. (E) Sickle RBC adhesion to heme-activated endothelial cells is significantly reduced by imatinib (5 μM) treatment, compared with control (vehicle, DMSO) treatment (N = 13 subjects, mean adhesion of untreated vs. imatinib-treated sickle cells ± SEM = 383 ± 57 vs. 171 ± 30, P < 0·001, paired t-test).). (RBC, red blood cell; HUVEC, human umbilical vein endothelial cells; HPMEC, human pulmonary microvascular endothelial cells).