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Inhibitory Effects of PD98059, SB203580, and SP600125 on α- and δ-granule Release and Intracellular Ca2+ Levels in Human Platelets
Biomed. Sci. Lett. 2018;24:253-262
Published online September 30, 2018;
© 2018 The Korean Society For Biomedical Laboratory Sciences.

Hyuk-Woo Kwon†,*

Department of Biomedical Laboratory Science, Far East University, Eumseong 27601, Korea
Correspondence to: Hyuk-Woo Kwon. Department of Biomedical Laboratory Science, Far East University, 76-32, Daehak-gil, Gamgok-myeon, Eumseong-gun, Chungcheongbuk-do 27601, Korea.
Tel: +82-43-880-3801, Fax: +82-43-880-3876, e-mail:
Received May 28, 2018; Revised August 29, 2018; Accepted August 29, 2018.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Platelets are activated at sites of vascular injury via several molecules, such as adenosine diphosphate, collagen and thrombin. Full platelet aggregation is absolutely essential for normal hemostasis. Moreover, this physiological event can trigger circulatory disorders, such as thrombosis, atherosclerosis, and cardiovascular disease. Therefore, platelet function inhibition is a promising approach in preventing platelet-mediated circulatory disease. Many studies reported the involvement of mitogen-activated protein kinases (MAPKs) signaling pathways in platelet functions. However, these studies were limited. Thus, we examined MAPK signaling pathways in human platelets using specific MAPK inhibitors, such as PD98059, SB203580, and SP600125. We observed that these inhibitors were involved in calcium mobilization and influx in human platelets. They also suppressed thrombin-induced α- and δ-granule release. These results suggest that PD98059, SB203580, and SP600125 exhibit Ca2+ antagonistic effects.
Keywords : MAPK signaling pathways, Calcium mobilization, Calcium influx, Granule release