The effect of in vitro activation and platelet interaction on the CD9 distribution and adhesion properties of human eosinophils

Fernvik, Eva; Lundahl, Joachim; Magnusson, Carl; Halldén, Gunilla

doi:10.1007/s000110050383

Cited by 16 publications

(11 citation statements)

References 19 publications

(26 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…50 Several authors have found decreasing CD9 expression in eosinophils on activation, a phenomenon probably caused by release/shedding of soluble forms of CD9 and not caused by intracellular degradation. 51,52 It is likely that this CD9 expression decrease could be due to secretion of CD9 1 eosinophil exosomes, and for this reason, we have observed an increase in CD9 1 exosomes after eotaxin eosinophil stimulation.…”

Section: Discussionmentioning

confidence: 76%

Exosome secretion by eosinophils: A possible role in asthma pathogenesis

Mazzeo

Cañas

Zafra

et al. 2015

Journal of Allergy and Clinical Immunology

106

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 76%

Exosome secretion by eosinophils: A possible role in asthma pathogenesis

Mazzeo

Cañas

Zafra

et al. 2015

Journal of Allergy and Clinical Immunology

106

View full text Add to dashboard Cite

“…Arterial thrombosis is a major pathogenic mechanism in acute coronary syndromes [127,128] and involves cross‐talk among platelets, leukocytes and endothelial cells [129]. A plethora of stimulatory or inhibitory agonists may influence the formation of platelet–leukocyte aggregates which may facilitate leukocyte tethering, rolling and migration and enhance thrombin generation [130,131]. Leukocyte‐released is one of the factors that could induce platelet–leukocyte aggregation [132].…”

Section: Oxidative Stress and Arterial Thrombosismentioning

confidence: 99%

Oxidative stress in atherogenesis and arterial thrombosis: the disconnect between cellular studies and clinical outcomes

Madamanchi

Hakim

Runge

2005

Journal of Thrombosis and Haemostasis

181

143

View full text Add to dashboard Cite

To cite this article: Madamanchi NR, Hakim ZS, Runge MS. Oxidative stress in atherogenesis and arterial thrombosis: the disconnect between cellular studies and clinical outcomes. J Thromb Haemost 2005; 3: 254-67.Summary. Atherosclerosis is a multifactorial disease for which the molecular etiology of many of the risk factors is still unknown. As no single genetic marker or test accurately predicts cardiovascular death, phenotyping for markers of inflammation may identify the individuals at risk for vascular diseases. Reactive oxygen species (ROS) are key mediators of signaling pathways that underlie vascular inflammation in atherogenesis, starting from the initiation of fatty streak development through lesion progression to ultimate plaque rupture. Various animal models of atherosclerosis support the notion that ROS released from NAD(P)H oxidases, xanthine oxidase, lipoxygenases, and enhanced ROS production from dysfunctional mitochondrial respiratory chain indeed have a causatory role in atherosclerosis and other vascular diseases. Human investigations also support the oxidative stress hypothesis of atherogenesis. This is further supported by the observed impairment of vascular function and enhanced atherogenesis in animal models that have deficiencies in antioxidant enzymes. The importance of oxidative stress in atherosclerosis is further emphasized because of its role as a unifying mechanism across many vascular diseases. The main contraindicator for the role oxidative stress plays in atherosclerosis is the lack of effectiveness of antioxidants in reducing primary endpoints of cardiovascular death and morbidity. However, this lack of effectiveness by itself does not negate the existence or causatory role of oxidative stress in vascular disease. Lack of proven markers of oxidative stress, which could help to identify a subset of population that can benefit from antioxidant supplementation, and the complexity and subcellular localization of redox reactions, are among the factors responsible for the mixed outcomes in the use of antioxidants for the prevention of cardiovascular diseases. To better understand the role of oxidative stress in vascular diseases, future studies should be aimed at using advances in mouse and human genetics to define oxidative stress phenotypes and link phenotype with genotype.

show abstract

“…To confirm that the collagen preparation does not activate leukocytes, platelet-poor blood was prepared by using Percoll (Amersham Pharmacia Biotech) as described previously 18 but omitting the step of red blood cell lysis. The lower layer (granulocytes and red blood cells) was resuspended with HEPES-buffered saline containing 1.25 mmol/L CaCl 2 and centrifuged at 800g for 10 minutes.…”

Section: Platelet-poor Blood Preparationmentioning

confidence: 99%

“…For example, plateletmonocyte conjugation may enhance thrombin generation, and conjugated platelets may facilitate leukocyte rolling, adhesion, and migration in vivo 17 and in vitro. 18 Previous studies have mostly been performed on isolated cells 19,20 and have thus neglected the possibly important influences of red blood cells and plasma components on these interactions. Studies in whole blood 21 were conducted in the presence of citrate, ie, with subphysiological calcium concentrations, which may alter platelet responses.…”

mentioning

confidence: 99%

Platelet-Leukocyte Cross Talk in Whole Blood

Lindqvist

et al. 2000

ATVB

191

145

View full text Add to dashboard Cite

Abstract-Thrombosis and inflammation involve complex platelet-leukocyte interaction, the details of which are not fully elucidated. Therefore, we investigated cross talk between platelets and leukocytes in whole blood, under the following physiological conditions: at 37°C, with normal calcium concentrations, and with shear force. Platelet P-selectin and leukocyte CD11b expression were used to monitor platelet and leukocyte activation, respectively, and platelet-leukocyte aggregation (PLA) was analyzed. The leukocyte-specific agonist N-formyl-methionyl-leucyl-phenylalanine (10 Ϫ6 mol/L) increased P-selectin-positive platelets from 2.5Ϯ0.1% to 5.1Ϯ0.6% (PϽ0.05). The increase was inhibited by either the platelet-activating factor (PAF) antagonist SR27417, the superoxide anion scavenger superoxide dismutase, the 5-lipoxygenase inhibitor Zileuton, or the 5-lipoxygenase-activating protein inhibitor MK-886, suggesting the involvement of PAF, superoxide anion, and 5-lipoxygenase products in leukocyte-induced platelet activation. The platelet-specific agonist collagen (1 g/mL) increased leukocyte CD11b expression from 2.

show abstract

The effect of in vitro activation and platelet interaction on the CD9 distribution and adhesion properties of human eosinophils

Abstract: Our findings, that CD9 expression on eosinophils is dynamically regulated, support our previous suggestion that CD9 may be a useful activity marker and that platelet interaction acts on eosinophil adhesion.

Cited by 16 publications

References 19 publications

Exosome secretion by eosinophils: A possible role in asthma pathogenesis

Exosome secretion by eosinophils: A possible role in asthma pathogenesis

Oxidative stress in atherogenesis and arterial thrombosis: the disconnect between cellular studies and clinical outcomes

Platelet-Leukocyte Cross Talk in Whole Blood

Contact Info

Product

Resources

About