Extended Data Fig. 1: The hydrogel-based thromboinflammation-on-a-chip model was maintained under microcirculatory flow conditions for at least two months and exhibited physiologically relevant microvascular barrier function.
From: Clinically relevant clot resolution via a thromboinflammation-on-a-chip
a, Computational fluid dynamics (CFD) simulation of the microchannels indicating the wall shear stress within the microchannels. b, A representative phase-contrast microscopy image of the microvasculature-on-a-chip during Step 1 in Fig. 1. c, A representative epifluorescence image of the engineered microvasculature after a 15-min perfusion of 70 kDa dextran-FITC demonstrates that the system is impermeable to dextran-FITC under physiological flow conditions during Step 1. in Fig. 1. d, Representative stitched-composite of epifluorescence images after a 15-min perfusion of 70 kDa dextran-FITC into the microvasculature inflamed by either 1 or 10 ng ml−1 TNF, demonstrate that TNF increases permeability in a dose-dependent manner. e, Quantitative analysis of the apparent permeability of the microvasculature after 16 h of stimulation with different doses of TNF. f, Representative confocal microscopy images show that endothelial-specific proteins VE-cadherin and PECAM−1 remain primarily located at cell-cell junction after two months of culture in the microvasculature-on-a-chip model. g, Representative confocal microscopy images show that endothelial cells continue to express VE-cadherin and PECAM-1 after 16 h of exposure to 10 ng ml−1 TNF, although these proteins become more diffusively distributed compared to the resting endothelium in (f). [Scale bar = 20 μm (f,g). n = 4 biologically independent replicates. Data are presented as mean values +/− SD. p values were calculated using one-way ANOVA with Tukey correction (e)].
