Lack of P-selectin glycoprotein ligand-1 protects mice from thrombosis after collagen/epinephrine challenge

Miszti-Blasius, Kornél; Debreceni, Ildikó Beke; Felszeghy, Szabolcs; Dezső, Balázs; Kappelmayer, János

doi:10.1016/j.thromres.2010.11.022

Cited by 21 publications

(19 citation statements)

References 41 publications

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“…Several studies were launched with this hypothesis and they unequivocally proved that the lack of this adhesive protein is indeed protective against induced arterial and venous thrombosis in murine models [66–68]. …”

Section: The Role Of Selectins and Psgl-1 In Thrombus Developmentmentioning

confidence: 99%

“…Subsequently, endothelial cells become activated by the accumulation of malignant cells and P-selectin-dependent platelet-tumor cell interactions. Hence, they show increased expression of E-selectin with induced production of different chemokines and facilitate the subsequent recruitment of monocytes and myeloid cells [66]. The blocking of E-selectin function attenuated liver [109] and lung metastases by colon carcinoma cells [110]; however, others found E-selectin dispensable in lung metastasis indicating its role merely in local activation of lung microvascular endothelial cells [80].…”

Section: The Role Of the Selectin-psgl-1 Axis In Malignanciesmentioning

confidence: 99%

“…The authors are indebted to Dr. Hendra Setiadi (Oklahoma City, OK, USA) for his critical comments. They would like to thank Elsevier Global Rights Department for permitting the use of Figures 2, 3, and 4 originally published by Miszti-Blasius et al [66], Dr. Péter Nagy (Department of Biophysics and Cell Biology, University of Debrecen) for helping in the CLSM analysis, and Dr. Bhattoa Harjit Pal (Department of Laboratory Medicine, University of Debrecen) for critically reviewing the manuscript.…”

Section: Acknowledgmentsmentioning

confidence: 99%

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The Interaction of Selectins and PSGL-1 as a Key Component in Thrombus Formation and Cancer Progression

Kappelmayer

Nagy

2017

BioMed Research International

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Cellular interaction is inevitable in the pathomechanism of human disease. Formation of heterotypic cellular aggregates, between distinct cells of hematopoietic and nonhematopoietic origin, may be involved in events leading to inflammation and the complex process of cancer progression. Among adhesion receptors, the family of selectins with their ligands have been considered as one of the major contributors to cell-cell interactions. Consequently, the inhibition of the interplay between selectins and their ligands may have potential therapeutic benefits. In this review, we focus on the current evidence on the selectins as crucial modulators of inflammatory, thrombotic, and malignant disorders. Knowing that there is promiscuity in selectin binding, we outline the importance of a key protein that serves as a ligand for all selectins. This dimeric mucin, the P-selectin glycoprotein ligand 1 (PSGL-1), has emerged as a major player in inflammation, thrombus, and cancer development. We discuss the interaction of PSGL-1 with various selectins in physiological and pathological processes with particular emphasis on mechanisms that lead to severe disease.

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Section: The Role Of Selectins and Psgl-1 In Thrombus Developmentmentioning

confidence: 99%

Section: The Role Of the Selectin-psgl-1 Axis In Malignanciesmentioning

confidence: 99%

Section: Acknowledgmentsmentioning

confidence: 99%

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The Interaction of Selectins and PSGL-1 as a Key Component in Thrombus Formation and Cancer Progression

Kappelmayer

Nagy

2017

BioMed Research International

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“…AECOPD and PE are associated with a wide range of inflammatory cells, mediators and cytokine network components, including P-selectin (11,12), inflammatory cytokines (13,14) and leucocytes (15,16). Previous studies have indicated that eosinophilic airway inflammation is also associated with the development of severe AECOPD (17)(18)(19).…”

Section: Introductionmentioning

confidence: 99%

Eosinophilic biomarkers for detection of acute exacerbation of chronic obstructive pulmonary disease with or without pulmonary embolism

Yang

Lü

Shu

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Eosinophilia has been implicated in the pathophysiology of acute exacerbation of chronic obstructive pulmonary disease (AECOPD). However, the role of eosinophil activation in the development of AECOPD remains unclear. In the present study, the reliability of plasma levels of eosinophil activation markers, including eosinophil cationic protein (ECP), major basic protein (MBP), eosinophil-derived neurotoxin (EDN) and eosinophil peroxidase (EPX), were measured and used as diagnostic biomarkers of AECOPD with or without pulmonary embolism (PE). A total of 47 patients with AECOPD, 30 patients with AECOPD/PE and 35 healthy adults were enrolled in the present study. Plasma levels of ECP, EDN, EPX and MBP were measured using commercial ELISA kits. The mean concentrations of plasma ECP, EDN, EPX and MBP in the patients with AECOPD was significantly 2.87-, 3.06-, 1.60-and 1.92-fold higher, respectively, compared with the control group (P<0.05). Similar results were obtained in patients with AECOPD/PE, for whom plasma levels of ECP, EDN, EPX and MBP were significantly 2.06-, 2.21-, 1.42-and 2.42-fold higher, respectively, compared with the controls (P<0.05). No significant differences were observed in the levels of these proteins between patients with AECOPD or AECOPD/PE. Among the four potential markers, ECP was determined to be the optimal marker for distinguishing patients with AECOPD or AECOPD/PE from the controls. No significant correlation was observed between marker concentrations and gender, age or disease severity. The results of the present study may have clinical applications in the diagnosis of AECOPD using these novel biomarkers.

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“…Many studies have investigated the association of the cell adhesion molecule P-selectin with blood coagulation and thrombosis [5–10]. P-selectin is partially responsible for the activation of platelets and the adhesion of certain leukocytes and platelets to the endothelium [11].…”

Section: Introductionmentioning

confidence: 99%

P-Selectin: An Unpredicted Factor for Deep Vein Thrombosis after Total Hip Arthroplasty

Shi

Nakamura

et al. 2014

BioMed Research International

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Introduction. Deep vein thrombosis (DVT) is a severe complication after total hip arthroplasty (THA). It leads to acute pulmonary embolism, a life-threatening disease. P-selectin is a 140-kDa transmembrane glycoprotein. Elevated P-selectin was associated with 1.7-fold increase in the risk of venous thrombosis. Materials and Methods. To confirm the association, a total of 91 subjects who received primary total hip arthroplasty using lateral approach performed by one skilled orthopedic surgeon were studied. All the patients were consecutively enrolled at the Center of Diagnosis and Treatment for Joint Diseases, Drum Tower Hospital affiliated to the Medical School of Nanjing University from 2010 to 2012. All the subjects received venography 3–5 days after operation. We measured P-selectin by means of a highly sensitive sandwich ELISA technique and a commercially available test reagent set. Results. No significant association was detected between P-selectin and DVT (all P values > 0.05). ΔsP-selectin was correlated with weight, APTT after operation, history of DVT, and diagnosis of primary disease ( P values were 0.03, 0.03, 0.04, and 0.02, resp.). Conclusion. P-selectin may not be a predicted factor for deep vein thrombosis after total hip arthroplasty.

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Lack of P-selectin glycoprotein ligand-1 protects mice from thrombosis after collagen/epinephrine challenge

Cited by 21 publications

References 41 publications

The Interaction of Selectins and PSGL-1 as a Key Component in Thrombus Formation and Cancer Progression

The Interaction of Selectins and PSGL-1 as a Key Component in Thrombus Formation and Cancer Progression

Eosinophilic biomarkers for detection of acute exacerbation of chronic obstructive pulmonary disease with or without pulmonary embolism

P-Selectin: An Unpredicted Factor for Deep Vein Thrombosis after Total Hip Arthroplasty

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