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Characterization of platelet function in cyclic hematopoietic dogs.
C D Lothrop1, R V Candler, H L Pratt
1University of Tennessee Department of Environmental Practice, College of Veterinary Medicine 37901-1071.
Experimental Hematology
|October 11, 1991
Summary
Platelets in cyclic hematopoietic (CH) dogs show defective aggregation with certain agonists, indicating a storage pool disease. This defect involves decreased phosphorylation of a 40-kd protein, impacting platelet function.
Area of Science:
- Hematology
- Biochemistry
- Canine Medicine
Background:
- Cyclic hematopoiesis (CH) is a disorder affecting blood cell production.
- Platelet function is crucial for hemostasis and thrombosis.
- Understanding platelet defects in CH dogs can provide insights into human platelet disorders.
Purpose of the Study:
- To compare platelet aggregation in normal and CH dogs using various agonists.
- To investigate biochemical differences in platelets from CH dogs.
- To identify the underlying defect in CH platelet dysfunction.
Main Methods:
- Platelet aggregation assays with eight different agonists.
- Radioimmunoassay (RIA) for Thromboxane B2 (TXB2) measurement.
- Analysis of serotonin and adenine nucleotide storage pools.
- Western blot analysis of protein phosphorylation.
Main Results:
- CH platelets exhibited defective aggregation with collagen, platelet-activating factor (PAF), and 12-O-tetradecanoyl phorbol-13-acetate (TPA).
- Aggregation was normal with ADP, phospholipase C (PLC), arachidonic acid plus epinephrine, and A23187.
- Homozygous CH dogs had decreased serotonin and adenine nucleotide storage pools.
- Collagen-stimulated phosphorylation of a 40-kd protein was reduced in CH platelets.
Conclusions:
- CH dogs possess a biochemical defect in platelets leading to storage pool disease.
- This defect is associated with impaired phosphorylation of a 40-kd protein upon collagen stimulation.
- Findings suggest a specific molecular abnormality contributing to platelet dysfunction in CH.