1. The anti-aggregatory potency of a number of E-type PGs was compared in human and rabbit platelet-rich plasma (PRP) and washed platelets. The potency of 13,14-dihydro-PGE1 and 5,6-dihydro-PGE3 is significantly higher in human than in rabbit washed platelets, while the potency of 15-keto-13,14-dihydro-PGE1 is higher in rabbit. 2. The potency of PGEs in rabbit PRP is very similar to that of washed platelets, with the exception of 1a,1b-dihomo-PGE2, which is of a significantly lower potency in PRR. 3. In human, 5,6-trans-PGE2, PGE3, and 15-keto-13,14-dihydro-PGE1 are more potent in PRP than in washed platelets. 4. The results indicate that the potency of E-type PGs in human and rabbit platelets is different and plasma can essentially influence the anti-aggregatory effect of PGEs; plasma can either decrease or increase potency.
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http://dx.doi.org/10.1016/0742-8413(93)90168-k | DOI Listing |
J Vis Exp
January 2025
Depeartment of Chemical and Biological Engineering, Colorado School of Mines; Quantitative Biosciences and Engineering, Colorado School of Mines;
Platelets are blood cells that play an integral role in hemostasis and the innate immune response. Platelet hyper- and hypoactivity have been implicated in metabolic disorders, increasing risk for both thrombosis and bleeding. Platelet activation and metabolism are tightly linked, with the numerous methods to measure the former but relatively few for the latter.
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February 2025
Shanghai-MOST Key Laboratory of Health and Disease Genomics, NHC Key Lab of Reproduction Regulation, Shanghai Institute for Biomedical and Pharmaceutical Technologies, Shanghai 200237, China.
Thromboxane A (TXA), a prothrombotic factor that induces platelet aggregation and thrombosis, acts as a vasoconstrictor by activating TXA receptors (TP receptors). TXA is extremely unstable and metabolizes into three major metabolites: 2,3-dinor thromboxane B (2,3-dinor-TXB), 11-dehydro TXB(11-dh-TXB), and 11-dehydro-2,3-dinor TXB(11-dh-2,3-dinor-TXB). 8-Iso-prostaglandin F(8-iso-PGF), a prostaglandin-like compound widely considered the best biomarker of oxidative stress, can also activate TP receptors.
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December 2024
Molecular Toxinology Lab, Research and Development Department, Ezequiel Dias Foundation-FUNED, Belo Horizonte 30510-010, MG, Brazil.
Spiders of the genus represent a public health problem in Brazil due to the severity of the cutaneous and systemic effects that may result from their bite. In the systemic form of loxoscelism, hemolytic anemia, thrombocytopenia, and disseminated intravascular coagulation can occur. Despite the seriousness of accidents, the venom of some species has not yet been properly characterized considering these hemotoxic effects, such as that of , , and .
View Article and Find Full Text PDFPlatelets
December 2024
Department of Immunology and Immunotherapy, College of Medicine and Health, University of Birmingham, Birmingham, UK.
Invasive non-typhoidal infections are responsible for >75 000 deaths/year and >500 000 cases/year globally. Seventy-five percent of these cases occur in Sub-Saharan Africa, an increasing number of which are from multi-drug resistant strains. Interactions between bacteria and platelets can lead to thrombus formation, which can be beneficial for control of infection (immunothrombosis), or harmful through uncontrolled inflammation and organ damage (thromboinflammation).
View Article and Find Full Text PDFJ Vis Exp
November 2024
Department of Haematology, University Hospital of Bordeaux; Inserm U1034, Biology of Cardiovascular Disease.
Activated platelets promote coagulation primarily by exposing the procoagulant phospholipid phosphatidylserine (PS) on their outer membrane surfaces and releasing PS-expressing microvesicles that retain the original membrane architecture and cytoplasmic components of their originating cells. The accessibility of phosphatidylserine facilitates the binding of major coagulation factors, significantly amplifying the catalytic efficiency of coagulation enzymes, while microvesicle release acts as a pivotal mediator of intercellular signaling. Procoagulant platelets play a crucial role in clot stabilization during hemostasis, and their increased proportion in the bloodstream correlates with an increased risk of thrombosis.
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