Effects of Platelet Transfusions: Plug Formation and Maintenance of Vascular Integrity

Roy, Albert J.; Djerassi, Isaac

doi:10.3181/00379727-139-36096

Cited by 38 publications

(17 citation statements)

References 6 publications

(8 reference statements)

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“…However, little is known about processes that determine barrier restoration or barrier protection. Platelets have been implicated in the maintenance of the vascular barrier, and proteins and lipids released after platelet activation have long been appreciated as enhancing the integrity of the microcirculation in vivo (17) and in vitro (42). In contrast, a reduction in circulating platelets (or thrombocytopenia) in humans accelerates capillary permeability, protein leakage, and edema formation in tissues (42), a result verified in animals (30,31,45).…”

Section: Discussionmentioning

confidence: 99%

Role of sphingosine-1 phosphate in the enhancement of endothelial barrier integrity by platelet-released products

Schaphorst

Chiang

Jacobs

et al. 2003

American Journal of Physiology-Lung Cellular and Molecular Phys

165

152

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In vitro and in vivo evidence indicates that circulating platelets affect both vascular integrity and hemostasis. How platelets enhance the permeability barrier of the vascular endothelium is not well understood. We measured the effect of isolated human platelets on human pulmonary artery endothelial cell (EC) barrier integrity by monitoring transmonolayer electrical resistance. EC barrier function was significantly increased by the addition of platelets (ϳ40% maximum, 2.5 ϫ 10 6 platelets/ml). Platelet supernatants, derived from 2.5 ϫ 10 6 platelets/ml, reproduced the barrier enhancement and reversed the barrier dysfunction produced by the edemagenic agonist thrombin, which implicates a soluble barrier-promoting factor. The barrier-enhancing effect of platelet supernatants was heat stable but was attenuated by either charcoal delipidation (suggesting a vasoactive lipid mediator) or pertussis toxin, implying involvement of a G i␣-coupled receptor signal transduction pathway. Sphingosine-1-phosphate (S1P), a sphingolipid that is released from activated platelets, is known to ligate G protein-coupled EC differentiation gene (EDG) receptors, increase EC electrical resistance, and reorganize the actin cytoskeleton (Garcia JG, Liu F, Verin AD, Birukova A, Dechert MA, Gerthoffer WT, Bamberg JR, and English D. J Clin Invest 108: [689][690][691][692][693][694][695][696][697][698][699][700][701] 2001). Infection of EC with an adenoviral vector expressing an antisense oligonucleotide directed against EDG-1 but not infection with control vector attenuated the barrier-enhancing effect of both platelet supernatants and S1P. These results indicate that a major physiologically relevant vascular barrier-protective mediator produced by human platelets is S1P. endothelium; lung; vasculature; injury; G protein; differentiation; cell differentiating gene THE VASCULAR ENDOTHELIUM IS a biologically complex tissue that forms a semipermeable barrier between the intravascular fluid compartment and the interstitium of various organs. Integrity of the endothelial cell (EC) monolayer is essential for homeostasis, and perturbations of the barrier function of the endothelium are now recognized as a cardinal feature of diverse and important pathobiological processes including acute lung injury and atherogenesis. The lung vasculature contains an enormous surface area and is particularly sensitive to the dynamic features of endothelial barrier dysregulation, where increased vascular permeability leads to exudation of fluid and solutes from the intravascular space into the pulmonary interstitium. Extensive increases in lung vascular permeability result in flooding of the alveolar air spaces (pulmonary edema), which is the hallmark pathophysiological derangement of the adult respiratory distress syndrome. Circulating blood platelets have been noted for many decades to be essential to the maintenance of the endothelium as a semipermeable barrier. In vitro and in vivo models have described profound defects in EC barrier function after perfusion wit...

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Section: Discussionmentioning

confidence: 99%

Role of sphingosine-1 phosphate in the enhancement of endothelial barrier integrity by platelet-released products

Schaphorst

Chiang

Jacobs

et al. 2003

American Journal of Physiology-Lung Cellular and Molecular Phys

165

152

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“…The other end of the umbilical vein was then cannulated with a blunt, hubless, 12 gauge needle shaft over which was slipped a 4 cm length of * in OD polyethylene tubing. 10 ml of 0.2% collagenase (type CLS, Worthington Biochemical Corp., Freehold, N.…”

Section: Methodsmentioning

confidence: 99%

“…(Abstr.) 12), and the response of the blood vessel to other physiologic and pathologic stimuli (13)(14)(15)(16)(17)(18)(19). Abnormalities of endothelial cell structure and function may contribute significantly to diseases of blood vessel walls such as thrombosis, atherosclerosis, and vasculitis (8,(17)(18)(19).…”

Section: Introductionmentioning

confidence: 99%

Culture of Human Endothelial Cells Derived from Umbilical Veins. IDENTIFICATION BY MORPHOLOGIC AND IMMUNOLOGIC CRITERIA

Jaffe¹,

Nachman²,

Becker³

et al. 1973

J. Clin. Invest.

6,457

2,694

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“…The physiologic importance of the S1P/SIP 1 pathway to maintenance of vascular barrier integrity is demonstrated by the protective role of platelets, which have long been known to decrease endothelial permeability (Gimbrone et al, 1969; Roy and Djerassi, 1972). Recently, our group identified S1P as the major barrier-protective product responsible for this effect within platelets (Schaphorst et al, 2003).…”

Section: S1p and S1p Receptorsmentioning

confidence: 99%

Regulation of vascular permeability by sphingosine 1-phosphate

Wang

Dudek

2009

Microvascular Research

152

165

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A significant and sustained increase in vascular permeability is a hallmark of acute inflammatory diseases such as acute lung injury (ALI) and sepsis and is an essential component of tumor metastasis, angiogenesis, and atherosclerosis. Sphingosine 1-phosphate (S1P), an endogenous bioactive lipid produced in many cell types, regulates endothelial barrier function by activation of its G-protein coupled receptor SIP1. S1P enhances vascular barrier function through a series of profound events initiated by SIP1 ligation with subsequent downstream activation of the Rho family of small GTPases, cytoskeletal reorganization, adherens junction and tight junction assembly, and focal adhesion formation. Furthermore, recent studies have identified transactivation of SIP1 signaling by other barrier enhancing agents as a common mechanism for promoting endothelial barrier function. This review summarizes the state of our current knowledge about the mechanisms through which the S1P/SIP1 axis reduces vascular permeability, which remains an area of active investigation that will hopefully produce novel therapeutic agents in the near future.

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Effects of Platelet Transfusions: Plug Formation and Maintenance of Vascular Integrity

Cited by 38 publications

References 6 publications

Role of sphingosine-1 phosphate in the enhancement of endothelial barrier integrity by platelet-released products

Role of sphingosine-1 phosphate in the enhancement of endothelial barrier integrity by platelet-released products

Culture of Human Endothelial Cells Derived from Umbilical Veins. IDENTIFICATION BY MORPHOLOGIC AND IMMUNOLOGIC CRITERIA

Regulation of vascular permeability by sphingosine 1-phosphate

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