The role of CaMKⅡδ in platelet activation mediated by thrombin and TRAP
10.13303/j.cjbt.issn.1004-549x.2025.10.002
- VernacularTitle:CaMKⅡδ在凝血酶及凝血酶受体激活肽介导的血小板活化中的作用
- Author:
Yafei ZHAO
1
;
Yongying CHEN
1
;
Pan SUN
1
;
Peng JIANG
1
;
Li MA
1
Author Information
1. Institute of Blood Transfusion, Chinese Academy of Medical Sciences & Peking Union Medical College, Chengdu 610052, China
- Publication Type:Journal Article
- Keywords:
platelets;
calcium signaling;
hemostasis;
PAR receptors;
CaMKⅡδ;
Hesperadin
- From:
Chinese Journal of Blood Transfusion
2025;38(10):1307-1312
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the role of calcium/calmodulin-dependent protein kinase Ⅱ delta (CaMKⅡδ) in platelet activation mediated by thrombin and thrombin receptor activator peptide (TRAP). Methods: The CaMKⅡδ-specific inhibitor Hesperadin was used to assess its inhibitory effects on platelet activation using multiple detection methods. These included: analyzing the inhibitory effect of different concentrations of Hesperadin on thrombin- and TRAP-induced platelet aggregation using a platelet aggregometer; measuring CD62P expression levels and calcium mobilization via flow cytometry; and determining dense granule release activity using a microplate reader. Results: Hesperadin at concentrations of 40 μM and 80 μM significantly inhibited thrombin- and TRAP-induced platelet aggregation (P<0.05). Within the concentration range of 20–80 μM, it significantly inhibited α-granule release and TRAP-induced calcium ion mobilization (P<0.05); at 80 μM, it markedly suppressed thrombin-induced platelet calcium ion mobilization and significantly inhibited dense granule release (P<0.05). Conclusion: The experimental results indicate that CaMKⅡδ in platelets is activated and plays a regulatory role in the process of platelet activation induced by thrombin and TRAP.
