Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.4.21.5 (
thrombin
)
33,306
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Complex disturbances in hemostasis characterise chronic renal insufficiency. Defect of primary hemostasis is a common cause of bleeding complications. The hemodialysis procedure (HD), by itself, influences platelet function (the key part of primary hemostasis) which is compromised after the procedure. Many functional defects of thrombocytes have been described in end stage renal failure (ESRF) patients; one of them is adhesion defect where the pivotal role plays the complex of glycoprotein Ib (GP Ib) and IX. The aim of the study was to determine the extent of activation, reactivity of platelets and expression of GP Ib in ESRF patients. The flow cytometry method was used, and
thrombin
was used for stimulation of thrombocytes. Membrane expression of GP Ib and
selectin P
was assessed in 14 hemodialysed patients before and after stimulation with
thrombin
, before and after HD and in 10 healthy persons. The patient group had lower expression of GP Ib on resting platelets and significantly lower expression of
selectin P
after stimulation with
thrombin
when compared to the control group. After HD, thrombocytes had much lower expression of GP Ib; however there was no difference in expression of
selectin P
when compared to the state before HD. A lower reduction of GP Ib expression after stimulation with
thrombin
was observed after and before HD. On the basis of the results the following conclusions may be drawn: hemo-dialysed ESRF patients have lower expression of platelet GP Ib and reactivity of thrombocytes; the HD results in further depression in expression of GP Ib and reactivity of thrombocytes. It is plausible that nitric oxide (NO) released during HD modulates the expression of
selectin P
, but it remains to be confirmed.
...
PMID:[Influence of hemodialysis on expression of glycoprotein lb platelets reactivity in patients with the end stage renal failure]. 1263 21
Platelet-leukocyte interactions represent an important determinant of the inflammatory response. Although mechanisms of platelet-neutrophil adhesion were studied extensively, little is known on the mechanisms of platelet-eosinophil interactions. The aim of the present study was to analyze the involvement of adhesion molecules and lipid mediators in platelet-eosinophil adhesion as compared to platelet-neutrophil adhesion. For that purpose human platelets, eosinophils and neutrophils were isolated and platelet-eosinophil and platelet-neutrophil adhesion induced by
thrombin
(30 mU/ml), LPS (0.01 microg/ml) and fMLP (1 microM) was quantified using the "rosettes" assay. The involvement of adhesion molecules such as
selectin P
, glycoprotein IIb/IIIa (GPIIb/IIIa) and lipid mediators such as of thromboxane A2 (TXA2), platelet activating factor (PAF) and cysteinyl leukotrienes (cysLTs) were studied using monoclonal antibodies and pharmacological inhibitors, respectively. Thrombin (30 mU/ml), LPS (0.01 microg/ml) and fMLP (1 microM) each of them induced platelet-eosinophil adhesion that was even more pronounced as compared with platelet-neutrophil adhesion induced by the same stimulus. Anti-CD62P antibody (1 microg/ml) and anti-GP IIb/IIIa antibody (abciximab-3 microg/ml) strongly inhibited platelet-eosinophil as well as platelet-neutrophil adhesion. Aspirin inhibited platelet-eosinophil adhesion, while MK 886-a FLAP inhibitor (10 microM), or WEB 2170-a PAF receptor antagonist (100 microM) were less active. On the other hand aspirin, MK 886 and WEB 2170 all three of them inhibited platelet-neutrophil adhesion. In summary, platelets adhered avidly to eosinophils both after activation of platelets by
thrombin
, eosinophils by fMLP or simultaneous activation of platelets and eosinophils by LPS. Similarly to platelet-neutrophil interaction adhesion of platelets to eosinophils involved not only adhesion molecules (
selectin P
, GPIIb/IIIa), but also lipid mediators such as TXA2. The involvement of PAF and cysteinyl leukotrienes in platelet-eosinophil adhesion was less pronounced as compared to platelet-neutrophil adhesion.
...
PMID:The involvement of adhesion molecules and lipid mediators in the adhesion of human platelets to eosinophils. 1639 20