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1 5-lipoxygenase-activating protein (FLAP) in human pulmonary microvascular endothelial cells.
2 an bone marrow endothelial cells and primary human pulmonary microvascular endothelial cells.
3 responses following HPAI virus infection of human pulmonary microvascular endothelial cells.
4 ative stress, survival, and proliferation of human pulmonary microvascular endothelial cells.
5 key enzyme in leukotriene formation, in both human pulmonary microvascular endothelial cells and a tr
7 and its receptors in the barrier function of human pulmonary microvascular endothelial cells and in n
8 oblasts, induced PAI-1 expression in primary human pulmonary microvascular endothelial cells and mono
9 bodies was performed using patient serum and human pulmonary microvascular endothelial cell cultures
10 studies demonstrated that ICAM-1 ligation on human pulmonary microvascular endothelial cells (ECs) se
12 sCD40L induces PMN-mediated cytotoxicity of human pulmonary microvascular endothelial cells (HMVECs)
14 cytokines on adhesion molecule expression on human pulmonary microvascular endothelial cells (HPMEC)
15 onents such as LPS mediate Ang2 signaling in human pulmonary microvascular endothelial cells (HPMECs)
16 To examine this hypothesis, we incubated human pulmonary microvascular endothelial cells (HPMVEC)
17 ET-1) and endothelin-B receptor (ET-BR) from human pulmonary microvascular endothelial cells (HPMVECs
18 itro migration of PMNs across a monolayer of human pulmonary microvascular endothelial cells in respo
19 Hypoxia stimulated gremlin secretion from human pulmonary microvascular endothelial cells in vitro
21 or necrosis factor-alpha (TNF-alpha)-treated human pulmonary microvascular endothelial cells (PMECs)
22 increased the permeability of monolayers of human pulmonary microvascular endothelial cells (PMVECs)
23 e used an in vitro transmigration model with human pulmonary microvascular endothelial cells (PMVECs)
25 ts of a VEGF receptor antagonist (SU5416) on human pulmonary microvascular endothelial cells under pu
26 on transendothelial electrical resistance of human pulmonary microvascular endothelial cells was anal
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