Intercellular Adhesion Molecule-1–Dependent Neutrophil Adhesion to Endothelial Cells Induces Caveolae-Mediated Pulmonary Vascular Hyperpermeability

Hu, Guochang; Vogel, Stephen M.; Schwartz, David E.; Malik, Asrar B.; Minshall, Richard D.

doi:10.1161/circresaha.107.167486

Cited by 112 publications

(138 citation statements)

References 46 publications

(44 reference statements)

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“…Significant increases in transcellular permeability can occur in conjunction with paracellular permeability as shown in murine models of endotoxin-induced acute respiratory distress syndrome, 61 or transcellular permeability can occur independently as seen during dengue virus infection 140 or HMGB1 stimulation of mouse lung microvascular endothelial cells in vitro. 141 Detailed analysis of clinical tissue samples for the activation of key signaling pathways associated with dissociation of junctions and transcytosis may provide additional insight into potential therapeutic targets.…”

Section: Imaging Studiesmentioning

confidence: 99%

“…60 Binding of ICAM-1 on human lung endothelial cells by neutrophils also leads to increased transcellular permeability through activation of caveolin-dependent albumin transport. 61 Interestingly, IRBC adhesion to ICAM-1 on a brain endothelial cell line (hCMEC/D3) has been linked to the formation of endothelial cup-like structures and trogocytosis of membrane fragments of IRBC, and the processes are associated with disruption of barrier integrity. 62 As endothelial docking structures or transmigrating cups are well described during leukocyte transmigration, 63 their formation around adherent IRBC that do not transmigrate is somewhat surprising.…”

Section: Cytoadherencementioning

confidence: 99%

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Dynamic interactions ofPlasmodiumspp. with vascular endothelium

Gillrie

2016

Tissue Barriers

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Plasmodial species are protozoan parasites that infect erythrocytes. As such, they are in close contact with microvascular endothelium for most of the life cycle in the mammalian host. The hostparasite interactions of this stage of the infection are responsible for the clinical manifestations of the disease that range from a mild febrile illness to severe and frequently fatal syndromes such as cerebral malaria and multi-organ failure. Plasmodium falciparum, the causative agent of the most severe form of malaria, is particularly predisposed to modulating endothelial function through either direct adhesion to endothelial receptor molecules, or by releasing potent host and parasite products that can stimulate endothelial activation and/or disrupt barrier function. In this review, we provide a critical analysis of the current clinical and laboratory evidence for endothelial dysfunction during severe P. falciparum malaria. Future investigations using state-of-the-art technologies such as mass cytometry and organs-on-chips to further delineate parasite-endothelial cell interactions are also discussed.

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Section: Imaging Studiesmentioning

confidence: 99%

Section: Cytoadherencementioning

confidence: 99%

Dynamic interactions ofPlasmodiumspp. with vascular endothelium

Gillrie

2016

Tissue Barriers

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“…22,23 Briefly, HUVECs expressing mouse ICAM-1 were washed once with EBM-2 and incubated with 15 g/mL rat anti-mouse ICAM-1 monoclonal antibody at room temperature for 20 minutes. Rat IgG2b was used as a control antibody.…”

Section: Icam-1 Crosslinkingmentioning

confidence: 99%

ICAM-1–activated Src and eNOS signaling increase endothelial cell surface PECAM-1 adhesivity and neutrophil transmigration

Liu¹,

Place²,

Chen³

et al. 2012

Blood

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Polymorphonuclear neutrophil (PMN) extravasation requires selectin-mediated tethering, intercellular adhesion molecule-1 (ICAM-1)–dependent firm adhesion, and platelet/endothelial cell adhesion molecule 1 (PECAM-1)–mediated transendothelial migration. An important unanswered question is whether ICAM-1–activated signaling contributes to PMN transmigration mediated by PECAM-1. We tested this concept and the roles of endothelial nitric oxide synthase (eNOS) and Src activated by PMN ligation of ICAM-1 in mediating PECAM-1–dependent PMN transmigration. We observed that lung PMN infiltration in vivo induced in carrageenan-injected WT mice was significantly reduced in ICAM-1−/− and eNOS−/− mice. Crosslinking WT mouse ICAM-1 expressed in human endothelial cells (ECs), but not the phospho-defective Tyr518Phe ICAM-1 mutant, induced SHP-2–dependent Src Tyr530 dephosphorylation that resulted in Src activation. ICAM-1 activation also stimulated phosphorylation of Akt (p-Ser473) and eNOS (p-Ser1177), thereby increasing NO production. PMN migration across EC monolayers was abolished in cells expressing the Tyr518Phe ICAM-1 mutant or by pretreatment with either the Src inhibitor PP2 or eNOS inhibitor L-NAME. Importantly, phospho–ICAM-1 induction of Src signaling induced PECAM-1 Tyr686 phosphorylation and increased EC surface anti–PECAM-1 mAb-binding activity. These results collectively show that ICAM-1–activated Src and eNOS signaling sequentially induce PECAM-1–mediated PMN transendothelial migration. Both Src and eNOS inhibition may be important therapeutic targets to prevent or limit vascular inflammation.

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“…Hypoxic conditions may profoundly affect endothelial cells through a cascade of reactions involving neutrophils (Sumagin et al, 2006(Sumagin et al, , 2008Butler et al, 2008;Carpenter and Alexander, 2008;Hu et al, 2008) and smooth muscle cells (Michiels et al, 2000;Aley et al, 2008;Jernigan et al, 2008;Mayr et al, 2008;Osada-Oka et al, 2008a, 2008bSheshgiri et al, 2008). Hypoxia regulates the expression of many genes, and the list of hypoxiarelated genes is growing (Yoshida et al, 2006;Eckardt et al, 2007;Said et al, 2007;Wang et al, 2007;Chen et al, 2008;Furuta et al, 2008;Yang et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Hypoxia induces Wee1 expression and attenuates hydrogen peroxide-induced endothelial damage in MS1 cells

Hong

Kim

et al. 2011

Exp Mol Med

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Abbreviations: cdc2, cell division cycle 2; cdk1, cycle dependent kinase 1; HIF-1α, hypoxia inducible factor-1α; Hsp, heat shock protein AbstractIn an oxygen-depleted environment, endothelial cells initiate an adaptive pattern of synthesis, which may enable them to survive hypoxic crises. Using high-resolution two-dimensional gel electrophoresis in conjunction with mass spectroscopy, we obtained a 24 differential display of proteins in the pancreatic endothelial cell line, MS-1, at four time points following induction of hypoxia. The induction of Wee1 under hypoxia was confirmed both at the mRNA and protein levels. The phosphorylation of cell division cycle 2, which is downstream of Wee1, was also increased after hypoxic exposure. In addition, pre-exposure to hypoxia attenuated a decrease in hydrogen peroxide-induced cell number. The induction of bax (a pro-apoptotic protein) and reduction of bcl (an anti-apoptotic protein) after hypoxia stimulus were also attenuated by hypoxic pre-exposure. Moreover, hydrogen peroxide-induced morphologic damage did not appear in the wild-type Wee1-expressing cells. Taken together, our results suggest that Wee1 may have important role in hypoxia-induced pathophysiological situations in endothelial cells.

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Intercellular Adhesion Molecule-1–Dependent Neutrophil Adhesion to Endothelial Cells Induces Caveolae-Mediated Pulmonary Vascular Hyperpermeability

Cited by 112 publications

References 46 publications

Dynamic interactions ofPlasmodiumspp. with vascular endothelium

Dynamic interactions ofPlasmodiumspp. with vascular endothelium

ICAM-1–activated Src and eNOS signaling increase endothelial cell surface PECAM-1 adhesivity and neutrophil transmigration

Hypoxia induces Wee1 expression and attenuates hydrogen peroxide-induced endothelial damage in MS1 cells

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