Activated Platelets and Endothelial Cell Interaction with Neutrophils under Flow Conditions.

Mine, Shinichiro; Fujisaki, Takeshi; Suematsu, Makoto; Tanaka, Yoshiya

doi:10.2169/internalmedicine.40.1085

Cited by 40 publications

(26 citation statements)

References 43 publications

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“…Expression of platelet surface α-granule P-selectin also is necessary for platelets to interact with neutrophils, monocytes, T cells and endothelium [21–23]. Neutrophils stimulated with LPS, on the other hand, shed microvesicles having potent platelet activating activity [24].…”

Section: Discussionmentioning

confidence: 99%

Platelet response as a sentinel marker of toll-like receptor 4 activation in mice

Jayachandran

Miller

Brunn

et al. 2010

Thrombosis Research

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Section: Discussionmentioning

confidence: 99%

Platelet response as a sentinel marker of toll-like receptor 4 activation in mice

Jayachandran

Miller

Brunn

et al. 2010

Thrombosis Research

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“…One possible mechanism involved in leukopenia includes the ability of platelets to interact with leukocytes and induce their so-called ˝secondary capture˝. The subsequent neutrophil-endothelial interaction could contribute to the initial decrease in leukocyte number and also trigger vascular inflammation [90,91].…”

Section: Leucopenia and Thrombocytopeniamentioning

confidence: 99%

Canine Babesiosis: Where Do We Stand?

et al. 2018

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Canine babesiosis is a tick-borne disease caused by protozoal haemoparasites of different Babesia species. Babesiosis is one of the most important globally extended and quickly spreading tick-borne infections of dogs. This comprehensive review gives an in-depth overview of Babesia species currently identifi ed in dogs together with relevant vector tick species and their geographical distribution, life cycle and transmission of parasite. The main mechanisms in the pathogenesis of babesiosis are described and elucidated by recent literature overview. As Babesia infection causes a disease with very variable clinical manifestations, special attention is given to clinical signs, laboratory features and clinicopathological fi ndings. The diagnosis of canine babesiosis by microscopy, serological and molecular methods is reviewed, together with recent advances in mass spectrometry based assays. Accurate detection and species recognition are important for the selection of the appropriate therapy, monitoring and prediction of the outcome of the disease. Finally, guidelines for the treatment and prevention of canine babesiosis are given.

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“…Recently, we demonstrated that FSS exposure was selective for Mac1 cleavage and occurred parallel to reduced binding of neutrophils to platelets and fibrinogen in suspension [8]. Fibrinogen is a Mac1 ligand that stabilizes neutrophil-platelet interactions [11]. Thus, FSS-induced ctsB release and Mac1 cleavage may serve to reduce or prevent neutrophil aggregate formation [8,12].…”

Section: Introductionmentioning

confidence: 98%

Fluid shear-induced cathepsin B release in the control of Mac1-dependent neutrophil adhesion

Akenhead

Fukuda

Schmid‐Schönbein

et al. 2017

Journal of Leukocyte Biology

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There is compelling evidence that circulatory hemodynamics prevent neutrophil activation, including adhesion to microvessels, in the microcirculation. However, the underlying mechanism or mechanisms by which that mechanoregulation occurs remain unresolved. Here, we report evidence that exposure to fluid shear stress (FSS) promotes neutrophils to release cathepsin B (ctsB) and that this autocrine regulatory event is antiadhesive for neutrophils on endothelial surfaces through Mac1-selective regulation. We used a combined cellengineering and immunocytochemistry approach to find that ctsB was capable of cleaving Mac1 integrins on neutrophils and demonstrated that this proteolysis alters their adhesive functions. Under no-flow conditions, ctsB enhanced neutrophil migration though a putative effect on pseudopod retraction rates. We also established a flow-based cell detachment assay to verify the role of ctsB in the control of neutrophil adhesion by fluid flow stimulation. Fluid flow promoted neutrophil detachment from platelet and endothelial layers that required ctsB, consistent with its fluid shear stress-induced release. Notably, compared with leukocytes from wild-type mice, those from ctsBdeficient (ctsB 2/2 ) mice exhibited an impaired CD18 cleavage response to FSS, significantly elevated baseline levels of CD18 surface expression, and an enhanced adhesive capacity to mildly inflamed postcapillary venules. Taken together, the results of the present study support a role for ctsB in a hemodynamic control mechanism that is antiadhesive for leukocytes on endothelium. These results have implications in the pathogenesis of chronic inflammation, microvascular dysfunction, and cardiovascular diseases involving sustained neutrophil activation in the blood and microcirculation.

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Activated Platelets and Endothelial Cell Interaction with Neutrophils under Flow Conditions.

Cited by 40 publications

References 43 publications

Platelet response as a sentinel marker of toll-like receptor 4 activation in mice

Platelet response as a sentinel marker of toll-like receptor 4 activation in mice

Canine Babesiosis: Where Do We Stand?

Fluid shear-induced cathepsin B release in the control of Mac1-dependent neutrophil adhesion

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