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. 2022 Jun 1;206(8):961–972. doi: 10.1164/rccm.202107-1774OC

Figure 3.

Figure 3.

Effect of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection on human lung microvascular endothelial cell (HMVEC) mediator secretion and proadhesive phenotype. (A) Concentrations of IL-6, IL-8, CCL-2, plasminogen activator inhibitor 1 (PAI-1), and vascular endothelial growth factor (VEGF) in supernatants of HMVECs from six different donors treated with medium or SARS-CoV-2 (multiplicity of infection [MOI] of 1; orange, strain nCoV/USA-WA1/2020). *P < 0.05, **P < 0.01, ***P < 0.001 by two-tailed Mann-Whitney U test. (B1) Histograms for CD102 (ICAM-2), CD31 (platelet endothelial cell adhesion molecule 1 [PECAM-1]), CD106 (vascular cell adhesion molecule 1 [VCAM-1]), CD144 (VE-cadherin), and CD62P (P-selectin) expression on HMVECs from four different donors after 24 hours of treatment with medium (gray) or infection with SARS-CoV-2 (MOI of 1; orange, strain nCoV/USA-WA1/2020). (B2) A double-gradient heat map of the relative mean fluorescence intensity on endothelial cells from four different donors after 24 hours of treatment with medium versus virus.