Coexpression of GMP-140 and PAF by endothelium stimulated by histamine or thrombin: a juxtacrine system for adhesion and activation of neutrophils.

Lorant, Diane E.; Patel, Kamala D.; McIntyre, Thomas M.; McEver, Rodger P.; Prescott, Stephen M.; Zimmerman, Guy A.

doi:10.1083/jcb.115.1.223

Cited by 564 publications

(331 citation statements)

References 67 publications

Supporting

Mentioning

307

Contrasting

Unclassified

Order By: Relevance

“…The presence of P-selectin on an activated endothelial cell layer plays an essential role in the initiation of a tentative adhesive interaction between the circulating inflammatory cell and activated endothelial cell monolayer [21]. Subsequently, the enhanced expression of endothelial cell-associated PAF has been shown to cause transient adherence of neutrophils to the endothelial cells [22][23][24].…”

Section: Resultsmentioning

confidence: 99%

Protease activation of calcium-independent phospholipase A2 leads to neutrophil recruitment to coronary artery endothelial cells

White¹,

McHowat²

2007

Thrombosis Research

View full text Add to dashboard Cite

Introduction-Thrombin or tryptase cleavage of protease-activated receptors (PAR) on human coronary artery endothelial cells (HCAEC) results in activation of a membrane-associated, calciumindependent phospholipase A 2 (iPLA 2 ) that selectively hydrolyzes plasmalogen phospholipids. Atherosclerotic plaque rupture results in a coronary ischemic event in which HCAEC in the ischemic area would be exposed to increased thrombin concentrations in addition to tryptase released by activated mast cells present in the plaque.

show abstract

Section: Resultsmentioning

confidence: 99%

Protease activation of calcium-independent phospholipase A2 leads to neutrophil recruitment to coronary artery endothelial cells

White¹,

McHowat²

2007

Thrombosis Research

View full text Add to dashboard Cite

show abstract

“…In response to stimuli such as histamine or LTC 4 , P-selectin is rapidly mobilized from storage granules known as Weibel-Palade bodies. 21,22 P-selectin expression can also be increased through de novo transcription and translation in response to agents such as TNF-␣. 23 In a recent study, 5 we showed that the central venules were incapable of responding to histamine or LTC 4 , suggesting a lack of the first mechanism.…”

Section: Discussionmentioning

confidence: 99%

Molecular mechanisms of tumor necrosis factor α-stimulated leukocyte recruitment into the murine hepatic circulation

2000

View full text Add to dashboard Cite

To date, much of the adhesion work in the liver has been restricted to sinusoids and postsinusoidal venules. However, selectins have been localized on the portal (presinusoidal) venules and these vessels have been shown to be important in metastasis of tumors. The purpose of this study was to characterize the leukocyte-endothelial interactions within the 3 compartments of the hepatic microvasculature under baseline conditions and in response to tumor necrosis factor ␣ (TNF-␣). Mice deficient in P-selectin or both E-and P-selectin were compared with wild-type (C57Bl/6, wild type) mice. Animals were injected with murine TNF-␣ (15 g/kg intraperitoneally [IP]) and the liver was examined by fluorescence intravital microscopy 4 hours later. Under baseline conditions, leukocyte flux in the portal venules was 1.42 ؎ 0.42 cells/min. Leukocyte flux in the portal venules of wild-type mice increased 8-fold in response to 4 hours of TNF-␣ stimulation. This was reduced by 50% in the P-selectin-deficient mice but was not reduced further by either the addition of an E-selectin antibody (9A9, 100 g intravenously [IV]) to these mice or in mice deficient in both E-and P-selectin. In P-selectindeficient mice, the addition of an antibody against ␣ 4 -integrin (R1-2, 75 g IP) reduced rolling to baseline. But in the E-and P-double-selectin-deficient mice the addition of an antibody against L-selectin (Mel 14, 3 g/kg IV) had no effect on TNF-␣-induced recruitment. Similar responses were seen in the central venules, however, in the sinusoids the increased number of stationary leukocytes seen in response to 4 hours of TNF-␣ stimulation in the wild-type mice was not reduced in P-selectin-deficient mice with or without the ␣ 4 -integrin antibody. These data suggest that leukocytes can use ␣ 4 -integrin independent of the selectins in the venules. Within the sinusoids, however, inhibition of E-selectin, P-selectin, and ␣ 4 -integrin was insufficient to reduce leukocyte recruitment. (HEPATOLOGY 2000;31:1123-1127.)The classic paradigm of inflammatory cell recruitment is a 4-step process involving initial tethering, rolling along the endothelium, followed by firm adhesion, then emigration out of the vasculature. Although the mechanisms of leukocyteendothelial cell interactions have been well characterized for vascular beds such as the mesentery, 1 the cremaster muscle, 2 and the dermis 3 of various species these tenets appear to not hold true for organs such as the liver. 4 In the narrow, low-flow sinusoidal circulation of the liver, tethering and rolling as a requirement for firm adhesion was not dependent on selectins. 4 Mediators such as LTC 4 or endotoxin, which induced selectin-dependent rolling in numerous vascular beds, induced selectin-independent adhesion in the sinusoids. 5,6 It is unclear whether this was a result of the low shear rates and physical trapping within the liver microcirculation or the fact that the selectins are not required for leukocyte-endothelial cell interactions in the liver. One possible explanation for a lack o...

show abstract

“…Alternatively, the PAF receptor may differ from CXCR2 in its PTX-sensitive signal transduction pathways and coupling to Gα proteins (48), which may enable a more rapid activation of Mac-1 adhesiveness under flow conditions. In parallel, endothelial PAF has been implicated in juxtacrine stimulation of integrin function in PMN tethered through P-selectin on thrombin-stimulated endothelium (54). Although P-selectin itself does not trigger arrest of PMN under flow, it may cooperate with chemoattractants to stimulate leukocytes (55).…”

Section: Involvement Of Platelet-activating Factor (Paf) and Leukotrimentioning

confidence: 99%

Effects of Oxidized Low Density Lipoprotein, Lipid Mediators and Statins on Vascular Cell Interactions

Weber¹,

Erl²,

Weber³

et al. 1999

CCLM

View full text Add to dashboard Cite

The integrin heterodimer CD11b/CD18 (␣M␤2, Mac-1, CR3) expressed on monocytes or polymorphonuclear leukocytes (PMN) is a receptor for iC3b, fibrinogen, heparin, and for intercellular adhesion molecule (ICAM)-1 on endothelium, crucially contributing to vascular cell interactions in inflammation and atherosclerosis. In this report, we summarize our findings on the effects of lipid mediators and lipid-lowering drugs. Exposure of endothelial cells to oxidized low density lipoprotein (oxLDL) induces upregulation of ICAM-1 and increases adhesion of monocytic cells expressing Mac-1. Inhibition experiments show that monocytes use distinct ligands, i.e. ICAM-1 and heparan sulfate proteoglycans for adhesion to oxLDL-treated endothelium. An albumin-transferable oxLDL activity is inhibited by the antioxidant pyrrolidine dithiocarbamate (PDTC), while 8-epi-prostaglandin F2␣ (8-epi-PGF2␣) or lysophosphatidylcholine had no effect, implicating yet unidentified radicals. Sequential adhesive and signaling events lead to the firm adhesion of rolling PMN on activated and adherent platelets, which may occupy areas of endothelial denudation. Shear-resistant arrest of PMN on thrombin-stimulated platelets in flow conditions requires distinct regions of Mac-1, involving its interactions with fibrinogen bound to platelet ␣IIb␤3, and with other platelet ligands. Both arrest and adhesion strengthening under flow are stimulated by platelet-activating factor and leukotriene B4, but not by the chemokine receptor CXCR2. We tested whether Mac-1-dependent monocyte adhesiveness is affected by inhibitors of hydroxy-methylglutaryl-Coenzyme A reductase (statins) which improve morbidity and survival of patients with coronary heart disease. As compared to controls, adhesion of isolated monocytes to endothelium ex vivo was increased in patients with hypercholesterolemia. Treatment with statins decreased total and low density lipoprotein (LDL) cholesterol plasma levels, surface expression of Mac-1, and resulted in a dramatic reduction of Mac-1-mediated monocyte adhesion to endothelium. The inhibition of monocyte adhesion was reversed by mevalonate but not LDL in vitro, indicating that isoprenoid precursors are crucial for adhesiveness of Mac-1. Such effects may crucially contribute to the clinical benefit of statins, independent of cholesterol-lowering, and may represent a paradigm for novel, anti-inflammatory mechanisms of action by this class of drugs.

show abstract

Coexpression of GMP-140 and PAF by endothelium stimulated by histamine or thrombin: a juxtacrine system for adhesion and activation of neutrophils.

Cited by 564 publications

References 67 publications

Protease activation of calcium-independent phospholipase A2 leads to neutrophil recruitment to coronary artery endothelial cells

Protease activation of calcium-independent phospholipase A2 leads to neutrophil recruitment to coronary artery endothelial cells

Molecular mechanisms of tumor necrosis factor α-stimulated leukocyte recruitment into the murine hepatic circulation

Effects of Oxidized Low Density Lipoprotein, Lipid Mediators and Statins on Vascular Cell Interactions

Contact Info

Product

Resources

About