Expression of ADP receptor P2Y12, thromboxane A2 receptor and C-type lectin-like receptor 2 in cord blood-derived megakaryopoiesis

Platelets ◽  
2020 ◽  
pp. 1-8
Author(s):  
Catharina Gerhards ◽  
Stefanie Uhlig ◽  
Mani Etemad ◽  
Foteini Christodoulou ◽  
Karen Bieback ◽  
...  
Keyword(s):  
Cord Blood ◽  
Thromboxane A2 ◽  
Thromboxane A2 Receptor ◽  
Adp Receptor

Deficiency of (33P)2MeS-ADP Binding Sites on Platelets with Secretion Defect, Normal Granule Stores and Normal Thromboxane A2 Production

1997 ◽  
Vol 77 (05) ◽  
pp. 0986-0990 ◽  
Author(s):  
Marco Cattaneo ◽  
Rossana Lombardi ◽  
Maddalena L Zighetti ◽  
Christian Gachet ◽  
Philippe Ohlmann ◽  
...  
Keyword(s):  
Binding Sites ◽  
Specific Binding ◽  
Thromboxane A2 ◽  
Normal Subjects ◽  
Congenital Defects ◽  
Normal Production ◽  
Adp Receptor ◽  
Partial Deficiency ◽  
Induced Aggregation ◽  
Platelet Secretion

SummaryBy the term “Primary Secretion Defect” (PSD), we mean a common heterogeneous group of congenital defects of platelet secretion, characterized by a normal primary wave of platelet aggregation induced by ADP and other agonists, a normal concentration of platelet granule contents, and normal production of thromboxane A2. The biochemical abnormalities responsible for PSD are not well known. Since a secretion defect similar to PSD is found in platelets that are severely deficient of binding sites for the ADP analogue 2MeS-ADP and do not aggregate in response to ADP, we tested the hypothesis that PSD platelets have moderately decreased 2MeS-ADP binding sites, which may be sufficient for normal ADP-induced aggregation but not for potentiating platelet secretion. The specific binding of [33P]2MeS-ADP to platelets from 3 PSD patients (347,443 and 490 sites/platelet; KD 2.8-3.9 nM) was lower than to platelets from 24 normal subjects (647 [530-1102]; KD = 3.8 [2.3-7.3]) (median [range]). Normal values were found in a fourth PSD patient (710; KD 3.7). The degree of inhibition of PGE1- induced cAMP increase by 0.1 |μM ADP was lower in patients than in controls. The secretion induced by the endoperoxide analogue U46619 from normal, acetylsalicylic acid-treated platelets under conditions that prevented the formation of large aggregates was potentiated by 1 fimol/1 ADP and inhibited by apyrase. These findings indicate that a partial deficiency of the platelet ADP receptor(s) might be responsible for the defect of platelet secretion in some PSD patients and that ADP potentiates platelet secretion independently of the formation of large aggregates and thromboxane A2 production.

Carrier-Mediated Active Transport of a Novel Thromboxane A2 Receptor Antagonist [2-(4-Chlorophenylsulfonylaminomethyl)indan-5-yl]acetate (Z-335) into Rat Liver

2002 ◽  
Vol 30 (5) ◽  
pp. 498-504 ◽  
Author(s):  
Yoshihiro Kawabata ◽  
Shigeru Furuta ◽  
Yutaka Shinozaki ◽  
Tadashi Kurimoto ◽  
Ryuichiro Nishigaki
Keyword(s):  
Receptor Antagonist ◽  
Active Transport ◽  
Rat Liver ◽  
Thromboxane A2 ◽  
Thromboxane A2 Receptor

scholarly journals Thromboxane A2 receptor blockade improves renal function and histopathology in the post-obstructive kidney

1994 ◽  
Vol 45 (1) ◽  
pp. 185-192 ◽  
Author(s):  
Craig A. Rinder ◽  
Perry V. Halushka ◽  
Mary Ann Sens ◽  
David W. Ploth
Keyword(s):  
Renal Function ◽  
Thromboxane A2 ◽  
Receptor Blockade ◽  
Thromboxane A2 Receptor

scholarly journals Flavonoids inhibit platelet function through binding to the thromboxane A2 receptor

2005 ◽  
Vol 3 (2) ◽  
pp. 369-376 ◽  
Author(s):  
J. A. GUERRERO ◽  
M. L. LOZANO ◽  
J. CASTILLO ◽  
O. BENAVENTE-GARCIA ◽  
V. VICENTE ◽  
...  
Keyword(s):  
Platelet Function ◽  
Thromboxane A2 ◽  
Thromboxane A2 Receptor

Lung injury in a surfactant-deficient lung is modified by indomethacin

1990 ◽  
Vol 69 (6) ◽  
pp. 2067-2071 ◽  
Author(s):  
R. Burger ◽  
D. Fung ◽  
A. C. Bryan
Keyword(s):  
Pulmonary Hypertension ◽  
Lung Injury ◽  
Thromboxane A2 ◽  
Neutrophil Infiltration ◽  
Lung Lavage ◽  
Thromboxane A2 Receptor ◽  
Beneficial Effects ◽  
Thromboxane Receptor ◽  
Pulmonary Arterial ◽  
Arterial Po2

Repetitive total lung lavage in adult rabbits leads to a reproducible severe surfactant-deficient lung injury. Hypoxemia requiring mechanical ventilation occurs, accompanied by a substantial pulmonary hypertension, a large intra-alveolar protein leak, peripheral neutropenia, and pathological features of marked neutrophil infiltration with extensive hyaline membrane formation. Pretreatment with indomethacin abolishes postlavage pulmonary hypertension, preserves a slightly better lung function with higher arterial PO2, and prevents the postlavage peripheral neutropenia found in untreated animals. Pretreatment with a thromboxane A2 receptor blocker (L 655,240, Merck Frosst, Canada) also completely attenuated pulmonary hypertension, providing evidence that thromboxane A2 mediates pulmonary arterial hypertension after lung lavage. However, specific thromboxane receptor blockade had no other long-lasting beneficial effects on the ongoing injury in this model.

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