Serotonin, norepinephrine, and histamine mediation of endothelial cell barrier function in vitro

Bottaro, Donald P.; Shepro, David; Peterson, Scott W.; Hechtman, Herbert B.

doi:10.1002/jcp.1041280208

Cited by 67 publications

(22 citation statements)

References 19 publications

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“…However, we cannot rule out that a receptor-mediated transcytotic pathway [30][31] may be in part responsible for this enhanced permeability of HUVEC monolayers. A similar retraction of endo thelial cells with formation of gaps in monolayers and an increase in permeability is observed in response to vasoactive amines [32][33][34][35] and PAF [11,36]. Clark ct al.…”

Section: Discussionmentioning

confidence: 80%

Tumor Necrosis Factor Alters Cytoskeletal Organization and Barrier Function of Endothelial Cells

Camussi

Turello

Bussolino

et al. 1991

Int Arch Allergy Immunol

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Treatment of human umbilical cord vein endothelial cells with tumor necrosis factor results in marked changes in cell shape and cytoskeletal organization. After 4 h of treatment, these cells loose reciprocal contacts with the formation of intercellular gaps. This retraction reaches a maximum after 6 h when most stress fibers staining for F-actin disappear and vinculin becomes diffused in the cytoplasm. Such changes spontaneously reverse after 24 h in the presence of tumor necrosis factor or after 2 h of incubation in fresh medium. After treatment with tumor necrosis factor, endothelial monolayers become permeable to albumin because of gaps that form between cells. Normal human serum, plasma α₁-proteinase inhibitor and an anti-inflammatory peptide that decrease synthesis of platelet-activating factor inhibit the changes induced by tumor necrosis factor. Furthermore, receptor antagonists of platelet-activating factor have the same effect. These findings suggest that platelet-activating factor is a secondary mediator responsible for the changes in cell shape and cytoskeletal organization, and for the leakiness of endothelial monolayers.

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Section: Discussionmentioning

confidence: 80%

Tumor Necrosis Factor Alters Cytoskeletal Organization and Barrier Function of Endothelial Cells

Camussi

Turello

Bussolino

et al. 1991

Int Arch Allergy Immunol

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“…44 The ability of BDMPs to pass through the endothelial barrier was measured in a transwell system, where confluent HUVECs cultured in the top chamber were first activated by histamine ( Figure 4D), which increases vascular permeability by inducing endothelial cells to contract. 45,46 BDMPs were then loaded onto the endothelial cells in the presence or absence of live or lyophilized platelets. After incubation for 3 hours at 37°C, the time when the highest level of BDMPs was found in the blood of FPI mice (Figure 1), BDMPs were detected in the bottom chamber when they were incubated with histamine-stimulated HUVECs and live, but not lyophilized, platelets ( Figure 4E).…”

Section: Bdmp Production By Injured Brain Cells and Transmigration Thmentioning

confidence: 99%

Brain-derived microparticles induce systemic coagulation in a murine model of traumatic brain injury

Tian

Salsbery

Wang

et al. 2015

Blood

141

186

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• Brain-derived cellular microparticles induce systemic coagulopathy in traumatic brain injury.• Platelets facilitate the transmigration of brain microparticles through the endothelial barrier into the circulation.Traumatic brain injury (TBI) is associated with coagulopathy, although it often lacks 2 key risk factors: severe bleeding and significant fluid resuscitation associated with hemorrhagic shock. The pathogenesis of TBI-associated coagulopathy remains poorly understood. We tested the hypothesis that brain-derived microparticles (BDMPs) released from an injured brain induce a hypercoagulable state that rapidly turns into consumptive coagulopathy. Here, we report that mice subjected to fluid percussion injury (1.9 6 0.1 atm) developed a BDMP-dependent hypercoagulable state, with peak levels of plasma glial cell and neuronal BDMPs reaching 17 496 6 4833/mL and 18 388 6 3657/mL 3 hours after TBI, respectively. Uninjured mice injected with BDMPs developed a dosedependent hyper-turned hypocoagulable state measured by a progressively prolonged clotting time, fibrinogen depletion, and microvascular fibrin deposition in multiple organs. The BDMPs were 50 to 300 nm with intact membranes, expressing neuronal or glial cell markers and procoagulant phosphatidylserine and tissue factor. Their procoagulant activity was greater than platelet microparticles and was dose-dependently blocked by lactadherin. Microparticles were produced from injured hippocampal cells, transmigrated through the disrupted endothelial barrier in a platelet-dependent manner, and activated platelets. These data define a novel mechanism of TBI-associated coagulopathy in mice, identify early predictive markers, and provide alternative therapeutic targets. (Blood. 2015;125(13):2151-2159

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“…[32][33][34]. Vecchio et al [23] demonstrated that the Ihiombin effect in increasing endothcliiil monolayer permeability was associated with an alteration in cell shape which corresponded with the dissolution of peripheral actin stress fibres.…”

Section: Combinations Of Tbe Cytokine Tnf and Acute Agonistsmentioning

confidence: 99%

Combinations of low concentrations of cytokines and acute agonists synergize in increasing the permeability of endothelial monolayers

Beynon

Haskard

Davies

et al. 1993

Clinical and Experimental Immunology

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SLMMARYThe deposition of circulating immune reactants in blood vessels, an important event in the pathogenesis of certain types of vasculitis, requires an increase in permeability in the endothelial monolayer. An in vitro model to examine the integrity of endothelial cell monolayers and their response to inflammatory mediators has been developed. Human umbiiieal vein endothelial cells were grown to confluence on an FITC-labellcd matrix and monolayer integrity was assessed by the exclusion of a '-M-anti-FITC antibody. Alteration in endothelial monolayer penneability was associated with an increase in uptake of '^^I-anti-FITC antibody, expressed as a percentage ofthe maximal uptake of antibody on to FITC-matdx frotn which endothelial cells had been stripped. We determined the effects on endothelial monolayer permeability of acute agonists (thrombin and histamine). cytokines (tumour necrosis factor-alpha (TNF-a). interferon-gamma (IFN-y), IL-I and IL-4) and combinations of acute agonists and cytokines. Addition of thrombin in concentrations ranging from 05 to 15 U/ml led to an increased uptake of'-'l-anti-FITC antibody from 2% to 15% relative to unstimulated endothelium. For other agonists and cyiokines the increases in permeability were: (i) histamine (50-400 pmo!/ml) increased uptake 5-22%: (ii) TNF (12 5-100 ng/ml) increased uptake 2-12%: (iii) IFN-7 (125-250 U/ml) inereased uptake I 5-3%. IL-l/i (50-100 U/ml) and U.-4 (50-100 U/ml) had no effect. Synergistic interactions on endothelial monolayer permeability were seen with the following combinations: (i) IL-4 (100 U/ml) and TNF (12-5 ng/ml) uptake 11 %; (ii) IL-4 (100 U/ml)and IFN-7 (125 U/ml) uptake6-5%; (iii)TNF(12-5ng/ml) and IFN-v (125 ng/ml) uptake 7%; (iv) thrombin (0 5 U/ml) and histamine (50 pmol/ml) uptake 13 5"/;,: and (v) TNF (12-5 ng/ml) and thrombin (0 5 U/ml) uptake 8 5'^. These observations suggest that interactions between cytokines and acute inflammatory mediators such as thrombin and histamine may be important in determining whether immune complexes are deposited in vessel walls. This model system may now be useful for the further investigation in vitro ofthe mechanisms involved in the pathogenesis of immune complex-mediated vascular damage.

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Serotonin, norepinephrine, and histamine mediation of endothelial cell barrier function in vitro

Cited by 67 publications

References 19 publications

Tumor Necrosis Factor Alters Cytoskeletal Organization and Barrier Function of Endothelial Cells

Tumor Necrosis Factor Alters Cytoskeletal Organization and Barrier Function of Endothelial Cells

Brain-derived microparticles induce systemic coagulation in a murine model of traumatic brain injury

Combinations of low concentrations of cytokines and acute agonists synergize in increasing the permeability of endothelial monolayers

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