Protein tyrosine phosphorylation in equine platelets: the effect of stimulation by thrombin and platelet-activating factor (PAF).
Abstract: Protein tyrosine phosphorylation (PTP) in thrombin- and platelet-activating factor (PAF)-stimulated equine platelet activation was investigated in the absence and presence of 2 protein tyrosine kinase inhibitors (PTKIs), methyl 2,5-dihydroxycinnamate (MDHC) and genistein. Washed equine platelets aggregated irreversibly in response to thrombin or PAF in an agonist concentration dependent fashion. MDHC produced an MDHC concentration and time dependent inhibitory effect on rate and extent of thrombin- and PAF-induced aggregations, whereas the effect of genistein on the same parameters was only genistein concentration dependent. Western blotting demonstrated tyrosine phosphorylated proteins in resting platelets. Changes in the PTP pattern occurred both when platelets were stimulated with varying concentrations of thrombin or PAF for a standard time (3 min) or with a standard agonist concentration (0.17 u/ml thrombin or 10(-10) mol/l PAF) for varying times. Different patterns of PTP were produced by thrombin and PAF. 500 mumol/l MDHC and 300 mumol/l genistein each affected the PTP patterns produced in response to thrombin or PAF, but in different ways. PTP results with thrombin and PAF in the presence of 500 mumol/l MDHC were similar, as were those in the presence of 300 mumol/l genistein. However, there were many differences in the PTP results between thrombin (or PAF) in the presence of MDHC and between thrombin (or PAF) in the presence of genistein. Therefore, although both inhibitors are PTKIs, they have different effects on the PTP induced by either agonist. Our work has produced the first evidence of PTP in equine platelets. It is probable that the changes in PTP are related to events in the signal transduction pathway.
Publication Date: 1995-11-01 PubMed ID: 8565942DOI: 10.1111/j.2042-3306.1995.tb04426.xGoogle Scholar: Lookup
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- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
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This research investigates how proteins within horse blood platelets react when stimulated by two clot-forming substances: thrombin and platelet-activating factor (PAF). The study found that the inhibitors, methyl 2,5-dihydroxycinnamate (MDHC) and genistein, interfered with clot formation, but differently.
An Overview of the Investigated Topic
- The research was centered around protein tyrosine phosphorylation (PTP), a chemical modification that occurs in proteins and plays a role in cellular processes like cell division and signal transduction. Specifically, the investigators focused on the effect of thrombin and platelet-activating factor (PAF) on PTP in equine (horse) platelets.
- Thrombin and PAF are both known as agonists, substances that initiate a physiological response when combined with a receptor – in this case, leading to platelet aggregation (clotting).
Methodology and Conduct of the Study
- The researchers worked with washed equine platelets and found that they clustered together (aggregated) in a concentration-dependent fashion when exposed to either thrombin or PAF.
- MDHC and genistein, both protein tyrosine kinase inhibitors (PTKIs), were introduced to observe their effect on the PTP process. They are known to inhibit or slow down the phosphorylation process, which in this case, would essentially slow down or stop the platelets from clumping together (clotting).
Key Findings of the Research
- Both MDHC and genistein affected the PTP process, but in different ways. The study revealed three distinct PTP patterns, altered by the concentration of thrombin or PAF, and by the amount and type of PTKI used. This indicated that although both MDHC and genistein are types of PTKIs, they had differing impacts on the thrombin- and PAF-induced aggregation and PTP process.
- The study provided the first evidence of PTP existing in equine platelets. This suggests that changes in PTP may be related to the processes in the signal transduction pathway, a chain of cellular events triggered by a signal interacting with a receptor.
Cite This Article
APA
Dillon AM, Heath MF.
(1995).
Protein tyrosine phosphorylation in equine platelets: the effect of stimulation by thrombin and platelet-activating factor (PAF).
Equine Vet J, 27(6), 448-458.
https://doi.org/10.1111/j.2042-3306.1995.tb04426.x Publication
Researcher Affiliations
- University of Cambridge, Department of Clinical Veterinary Medicine, UK.
MeSH Terms
- Animals
- Blood Platelets / drug effects
- Blood Platelets / metabolism
- Blotting, Western
- Cinnamates / pharmacology
- Dose-Response Relationship, Drug
- Electrophoresis, Polyacrylamide Gel
- Genistein
- Horses / blood
- Horses / physiology
- Isoflavones / pharmacology
- Luminescent Measurements
- Phosphorylation
- Platelet Activating Factor / pharmacology
- Platelet Aggregation / drug effects
- Platelet Aggregation / physiology
- Protein-Tyrosine Kinases / antagonists & inhibitors
- Protein-Tyrosine Kinases / metabolism
- Thrombin / pharmacology
- Time Factors
Citations
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