Polymorphonuclear leukocyte: arachidonate edema

1985 ◽  
Vol 59 (1) ◽  
pp. 47-55 ◽  
Author(s):  
D. M. Shasby ◽  
S. S. Shasby ◽  
M. J. Peach
Keyword(s):  
Endothelial Cells ◽  
Polymorphonuclear Leukocytes ◽  
Inflammatory Process ◽  
Capillary Permeability ◽  
Endothelial Permeability ◽  
Lung Edema ◽  
Potential Significance ◽  
Cyclooxygenase Activity ◽  
Alveolar Capillary ◽  
Cells Cultured

Polymorphonuclear leukocytes (PMN) are important participants in many models of acute lung edema. Enhanced metabolism of arachidonate is also characteristic of many of these models. We found that PMN and arachidonate, but neither alone, increased alveolar capillary permeability of isolated perfused lungs and increased transfer of albumin across monolayers of endothelial cells cultured on micropore filters. Inhibition of PMN, but not endothelial cyclooxygenase, blunted the edematous process. Neither PMN proteases nor PMN-derived oxidants were involved. The edemagenic activity was not found in supernatants of PMN and arachidonate, and unstable prostaglandins did not alter endothelial albumin transfer. The edemagenic process was not inhibited by blocking leukotriene synthesis, and endothelial albumin transfer was not increased by direct addition of leukotrienes to endothelium. These data demonstrate that PMN and arachidonate can interact to increase endothelial permeability and that PMN cyclooxygenase activity is important for this process. This interaction is of potential significance to the acute inflammatory process in the lung vasculature.

Adenosine 3',5'-cyclic monophosphate attenuates neutrophil-mediated increase in endothelial permeability

1993 ◽  
Vol 264 (2) ◽  
pp. H370-H375 ◽  
Author(s):  
A. Siflinger-Birnboim ◽  
D. C. Bode ◽  
A. B. Malik
Keyword(s):  
Endothelial Cells ◽  
Clearance Rate ◽  
Polymorphonuclear Leukocytes ◽  
Endothelial Permeability ◽  
H2o2 Production ◽  
Camp Concentration ◽  
Cyclic Monophosphate ◽  
Endothelial Monolayers ◽  
Albumin Clearance ◽  
Permeability Alterations

We studied the effects of 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP) and cholera toxin (CT) on 125I-labeled albumin flux across confluent monolayers of bovine pulmonary microvessel endothelial cells (BMVEC) grown on polycarbonate filters (10(5) BMVEC/filter). 8-BrcAMP and CT increased endothelial adenosine 3',5'-cyclic monophosphate (cAMP) concentrations about twofold. Polymorphonuclear leukocytes (PMN) were layered on BMVEC monolayers (ratio of 10:1) and activated with phorbol 12-myristate 13 acetate (PMA; 5 x 10(-9) M). Transendothelial 125I-labeled albumin clearance rate was measured to determine the endothelial permeability alterations. Activation of PMN in control monolayers resulted in an increase in transendothelial 125I-labeled albumin clearance rate from 0.090 +/- 0.011 to 0.37 +/- 0.06 microliters/min (P < 0.01). Treatment of endothelial monolayers with 8-BrcAMP (10(-3) M) significantly attenuated the increase in endothelial permeability after PMN activation (transendothelial 125I-labeled albumin clearance rate increased to 0.19 +/- 0.03 microliters/min; P < 0.01). Pretreatment of BMVEC monolayers with CT (10(-8) M) for 3 h before PMN activation prevented the PMN-mediated increase in endothelial permeability (125I-labeled albumin clearance rate only increased to 0.13 +/- 0.018 microliters/min). To simulate the effect of PMN activation, hydrogen peroxide (H2O2) was added directly onto BMVEC; both 8-BrcAMP and CT were shown to reduce the H2O2-mediated increase in endothelial permeability. 8-BrcAMP and CT pretreatment did not prevent PMN adhesion to BMVEC monolayer and superoxide anion and H2O2 production after PMA activation of PMN. We conclude that increased endothelial cAMP concentration prevents PMN-mediated endothelial injury by an action of the cyclic nucleotide on endothelial cells.

Thrombin Inhibition and Thrombin Generation by Cultured Aortic Endothelial and Smooth Muscle Cells from Minipig

1982 ◽  
Vol 48 (01) ◽  
pp. 101-103 ◽  
Author(s):  
B Kirchhof ◽  
J Grünwald
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vessel Wall ◽  
Thrombin Generation ◽  
Muscle Cells ◽  
Thrombin Inhibition ◽  
Generating Capacity ◽  
Wall Interaction ◽  
Cells Cultured

SummaryEndothelial and smooth muscle cells cultured from minipig aorta were examined for their inhibitory activity on thrombin and for their thrombin generating capacity.Endothelial cells showed both a thrombin inhibition and an activation of prothrombin in the presence of Ca++, which was enhanced in the presence of phospholipids. Smooth muscle cells showed an activation of prothrombin but at a lower rate. Both coagulation and amidolytic micro-assays were suitable for studying the thrombin-vessel wall interaction.

Signal transduction and regulation of lung endothelial cell permeability. Interaction between calcium and cAMP

1998 ◽  
Vol 275 (2) ◽  
pp. L203-L222 ◽  
Author(s):  
Timothy M. Moore ◽  
Paul M. Chetham ◽  
John J. Kelly ◽  
Troy Stevens
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Intracellular Signaling ◽  
Endothelial Permeability ◽  
Cell Permeability ◽  
Gap Formation ◽  
Pulmonary Endothelium ◽  
Intracellular Signals ◽  
Endothelial Cell Permeability ◽  
Cell Cell

Pulmonary endothelium forms a semiselective barrier that regulates fluid balance and leukocyte trafficking. During the course of lung inflammation, neurohumoral mediators and oxidants act on endothelial cells to induce intercellular gaps permissive for transudation of proteinaceous fluid from blood into the interstitium. Intracellular signals activated by neurohumoral mediators and oxidants that evoke intercellular gap formation are incompletely understood. Cytosolic Ca2+ concentration ([Ca2+]i) and cAMP are two signals that importantly dictate cell-cell apposition. Although increased [Ca2+]ipromotes disruption of the macrovascular endothelial cell barrier, increased cAMP enhances endothelial barrier function. Furthermore, during the course of inflammation, elevated endothelial cell [Ca2+]idecreases cAMP to facilitate intercellular gap formation. Given the significance of both [Ca2+]iand cAMP in mediating cell-cell apposition, this review addresses potential sites of cross talk between these two intracellular signaling pathways. Emerging data also indicate that endothelial cells derived from different vascular sites within the pulmonary circulation exhibit distinct sensitivities to permeability-inducing stimuli; that is, elevated [Ca2+]ipromotes macrovascular but not microvascular barrier disruption. Thus this review also considers the roles of [Ca2+]iand cAMP in mediating site-specific alterations in endothelial permeability.

Mechanisms leading to lung edema in pulmonary embolization

1960 ◽  
Vol 198 (3) ◽  
pp. 543-546 ◽  
Author(s):  
S. A. Kabins ◽  
J. Fridman ◽  
J. Neustadt ◽  
G. Espinosa ◽  
L. N. Katz
Keyword(s):  
Pulmonary Edema ◽  
Capillary Permeability ◽  
Lysergic Acid ◽  
Lung Edema ◽  
Pulmonary Infarction ◽  
Edema Formation ◽  
Lung Lobe ◽  
Pulmonary Embolization ◽  
Sympathetic Nervous ◽  
Lung Lobes

A localized pulmonary infarction was produced by injecting a starch suspension into the pulmonary artery wedge position of one lung lobe in pentobarbitalized dogs, and the effect of three so-called antiserotonins on the ensuing pulmonary edema was determined. Edema was inhibited in the nonembolized lung lobes in 88% of the B.A.S. (1-benzyl-2-methyl-5-methoxytryptamine HCl), 45% of the DHE (dihydroergotamine), and 12% of the BOL (2-brom- d-lysergic acid diethylamide) dogs. Reasons are given for assuming that the actions of B.A.S. and DHE are due to their antiadrenergic rather than to any antiserotonin properties which they may have. Serotonin, therefore, at most has a slight role in the pulmonary edema formation caused by starch emboli. It is postulated that the emboli by producing an infarct and setting up a reflex mediated through the sympathetic nervous system, cause the release in turn of catecholamines and of histamine, the latter being immediately responsible for the capillary permeability change leading to pulmonary edema.

scholarly journals Iron Uptake in Blood-Brain Barrier Endothelial Cells Cultured in Iron-Depleted and Iron-Enriched Media

2002 ◽  
Vol 71 (3) ◽  
pp. 1134-1140 ◽  
Author(s):  
W. Van Gelder ◽  
M. I. E. Huijskes-Heins ◽  
M. I. Cleton-Soeteman ◽  
J. P. Van Dijk ◽  
H. G. Van Eijk
Keyword(s):  
Endothelial Cells ◽  
Blood Brain Barrier ◽  
Iron Uptake ◽  
Brain Barrier ◽  
Blood Brain ◽  
Cells Cultured

Tissue inhibitor of metalloproteinases (TIMP) regulates extracellular type I collagen degradation by chondrocytes and endothelial cells

1987 ◽  
Vol 87 (2) ◽  
pp. 357-362
Author(s):  
J. Gavrilovic ◽  
R.M. Hembry ◽  
J.J. Reynolds ◽  
G. Murphy
Keyword(s):  
Endothelial Cells ◽  
Type I Collagen ◽  
Model System ◽  
Collagen Degradation ◽  
Type I ◽  
Tissue Inhibitor Of Metalloproteinases ◽  
Regulatory Factor ◽  
Tissue Inhibitor ◽  
Cells Cultured

A specific antiserum to purified rabbit tissue inhibitor of metalloproteinases (TIMP) was raised in sheep, characterized and used to investigate the role of TIMP in a model system. Chondrocytes and endothelial cells cultured on 14C-labelled type I collagen films and stimulated to produce collagenase were unable to degrade the films unless the anti-TIMP antibody was added. The degradation induced was inhibited by a specific anti-rabbit collagenase antibody. It was concluded that TIMP is a major regulatory factor in cell-mediated collagen degradation.

Matrigel induces thymosin beta 4 gene in differentiating endothelial cells

1995 ◽  
Vol 108 (12) ◽  
pp. 3685-3694 ◽  
Author(s):  
D.S. Grant ◽  
J.L. Kinsella ◽  
M.C. Kibbey ◽  
S. LaFlamme ◽  
P.D. Burbelo ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Basement Membrane ◽  
Morphological Differentiation ◽  
Tube Formation ◽  
Vessel Formation ◽  
Thymosin Beta 4 ◽  
Cdna Hybridization ◽  
Matrix Components ◽  
Cells Cultured

We performed differential cDNA hybridization using RNA from endothelial cells cultured for 4 hours on either plastic or basement membrane matrix (Matrigel), and identified early genes induced during the morphological differentiation into capillary-like tubes. The mRNA for one clone, thymosin beta 4, was increased 5-fold. Immunostaining localized thymosin beta 4 in vivo in both growing and mature vessels as well as in other tissues. Endothelial cells transfected with thymosin beta 4 showed an increased rate of attachment and spreading on matrix components, and an accelerated rate of tube formation on Matrigel. An antisense oligo to thymosin beta 4 inhibited tube formation on Matrigel. The results suggest that thymosin beta 4 is induced and likely involved in differentiating endothelial cells. Thymosin beta 4 may play a role in vessel formation in vivo.

Role of Leukocytes and Endothelial Cells in the Development of Angiogenesis in Inflammation and Wound Healing

2001 ◽  
Vol 125 (1) ◽  
pp. 67-71 ◽  
Author(s):  
Mark W. Lingen
Keyword(s):  
Wound Healing ◽  
Endothelial Cells ◽  
Blood Vessels ◽  
Peripheral Blood ◽  
Inflammatory Process ◽  
Signs And Symptoms ◽  
Critical Component ◽  
Complex Environment ◽  
Seminal Article

Abstract The basic signs and symptoms of inflammation and wound healing have been appreciated for thousands of years. However, the specific cells involved and their roles in this complex environment are still being elucidated today. In 1926, the origin of the phagocytic mononuclear ameboid wandering cell (macrophage) had not been determined. One popular theory was that the cells were differentiated from the endothelial cells of the nearby blood vessels, whereas others believed that the cells came from the peripheral blood or resting wandering cells. The purpose of this article is to review the seminal article published by Lang regarding this topic nearly 75 years ago. In addition, this article will review what is now known with regard to the role of the macrophage and endothelial cells in the development of angiogenesis, which is arguably the most critical component of successful inflammatory process or wound healing.

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