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Updated: Apr 19, 2026

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
Published on: May 23, 2025
Platelet apoptosis in patients with acute coronary syndromes
1Department of Internal Medicine, Zaozhuang Fourth Municipal, Zaozhuang, 277100, Shandong Province, P.R.China, spring201312@126.com.
Insights
Platelets from acute coronary syndrome (ACS) patients show signs of apoptosis, potentially explaining bleeding complications. Antioxidants like NAC and DTT reduced this platelet apoptosis in vitro.
Area of Science:
- Cardiovascular Biology
- Hematology
- Cellular Biology
Background:
- Platelet apoptosis is observed under various stimuli.
- Acute coronary syndrome (ACS) is a significant cardiovascular disease associated with bleeding complications.
- Platelet apoptosis may contribute to bleeding in ACS patients.
Purpose of the Study:
- To investigate the presence of apoptotic platelets in patients with ACS.
- To explore the mechanisms of platelet apoptosis in ACS.
- To assess the effect of antioxidants on platelet apoptosis in ACS.
Main Methods:
- Analysis of apoptotic markers in platelets from ACS patients and healthy donors using Western blot and flow cytometry.
- Assessment of phosphatidylserine exposure, mitochondrial membrane potential, and caspase-3 activation.
- Incubation of healthy platelets with platelet-poor plasma (PPP) from ACS patients.
- Evaluation of antioxidant effects (NAC, DTT) on platelet apoptosis.
Main Results:
- ACS patients exhibited increased platelet mitochondrial inner membrane potential depolarization, elevated Bax/Bak, and decreased Bcl-2/Bcl-XL.
- Caspase-3 activation and phosphatidylserine exposure were observed in platelets from ACS patients.
- Normal platelets incubated with ACS-PPP showed apoptotic events, which were reduced by NAC and DTT.
Conclusions:
- Platelets from ACS patients undergo apoptosis.
- ACS-derived PPP induces apoptosis in healthy platelets.
- Antioxidants NAC and DTT can mitigate ACS-induced platelet apoptosis in vitro.
Abstract:
Platelet apoptosis occurs commonly under various conditions such as physical and chemical stimuli. Acute coronary syndrome (ACS), one of most important cardiovascular and cerebrovascular diseases, severely threats people's health and is usually accompanied with various complications especially bleeding. There might be platelet apoptosis in ACS, which might be responsible for the complication of bleeding. The objective of the present study was to explore whether there were apoptotic platelets in ACS patients. Vein blood was drawn from eleven ACS patients and eleven health people. Platelet-rich plasma was prepared and subjected to apoptotic events analysis including increased expression of pro-apoptotic proteins and decreased expression of anti-apoptotic proteins, exposure of phosphatidylserine (PS), mitochondrial inner membrane potential depolarization and caspase-3 activation by Western blot and flow cytometry. In addition, washed platelets from the normal people were prepared and treated with the platelet-poor plasma (PPP) of the ACS patients, and were further examined apoptotic cascades. Paired Student's t test was used in the data comparisons. There were more platelets with depolarized mitochondrial inner membrane potential in the ACS patients than those of the health donors. Levels of Bax and Bak increased, while expression of Bcl-2 and Bcl-XL decreased in platelets from ACS patients. Caspase-3 activation was observed in platelets from the patients with ACS. Interestingly, there were significant differences in PS exposure between the platelets from the ACS patients and the normal controls. Furthermore, apoptotic events were observed in the normal platelets incubated with PPP from the ACS patients. In addition, pretreatment of healthy platelets with anti-oxidants N-acetyl cysteine (NAC) or dithiothreitol (DTT) significantly reduced ACS patients-derived PPP-induced platelet apoptosis. Platelets from the ACS patients are incurred apoptosis. Antioxidants NAC or DTT can reduce ACS patients-derived PPP-induced platelet apoptosis in vitro.
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