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An Antithrombotic Strategy by Targeting Phospholipase D in Human Platelets
Wan Jung Lu1,2,3, Chi Li Chung4,5, Ray Jade Chen6,7
1Department of Medical Research, Taipei Medical University Hospital, Taipei 110, Taiwan. luwj@tmu.edu.tw.
Journal of Clinical Medicine
|November 17, 2018
Summary
Phospholipase D (PLD) enzymes are vital for human platelet activation, unlike in mice. Targeting PLD1 and PLD2 offers a potential therapeutic strategy for preventing blood clots.
Area of Science:
- Biochemistry
- Hematology
- Pharmacology
Background:
- Phospholipase D (PLD) participates in diverse biological functions.
- PLD1 regulates mouse platelet activity, but its role in human platelet activation is unknown.
Purpose of the Study:
- To investigate the role of PLD in human platelet activation.
- To compare the function of PLD in human and mouse platelets.
Main Methods:
- Pharmacological inhibition of PLD1 and PLD2 in human platelets.
- Comparison with mouse platelet aggregation and thrombus formation studies (in vitro and in vivo).
Main Results:
- PLD1 and PLD2 inhibition significantly reduced human platelet aggregation, activation, adhesion, spreading, and clot retraction.
- Pharmacological inhibition did not affect mouse platelet aggregation in vitro, but PLD1 inhibition delayed in vivo thrombus formation.
- PLD plays distinct roles in human versus mouse platelet function.
Conclusions:
- PLD1 and PLD2 are essential for human platelet activation.
- Targeting PLD may offer a therapeutic approach for thromboembolic disorders.
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