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KMID : 1144820210270030170
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대한의생명과학회지
2021 Volume.27 No. 3 p.170 ~ p.176
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Thapsigargin Induces Platelet Aggregation, thereby Releases Lactate Dehydrogenase from Rat Platelets
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Baik Ji-Sue
Seo You-Na
Rhee Man-Hee
Park Moon-Taek
Kim Sung-Dae
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Abstract
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Thapsigargin (TG), a sarco/endoplasmic reticulum (ER) Ca2+-ATPase (SERCA) inhibitor, has been widely used as an agonist for platelet aggregation for decades. In this study, we investigated the effect of TG on the release of lactate dehydrogenase (LDH) for platelets and elucidated its mechanism. Platelet LDH release and platelet aggregation were increased by TG treatment; 1,000 nM of TG induced the complete lysis of platelets. Other agonists such as collagen (2.5 μg/mL), thrombin (0.1 U/mL), and ADP (10 mM) did not induce significant platelet LDH release despite platelet aggregation. Finally, we investigated the effects of pharmacological inhibitors on TG-induced platelet aggregation and LDH release. SP600125, a JNK inhibitor, and LY294002, a PI-3K inhibitor, inhibited TG-induced platelet LDH release but not platelet aggregation. Forskolin, an adenylyl cyclase activator, also inhibited LDH release without affecting platelet aggregation by TG. These results suggest that the TG-induced platelet aggregation was accompanied by LDH release but regulated by a different signaling pathway.
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KEYWORD
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Platelets, Thapsigargin, Lactate dehydrogenase, cAMP, JNK, PI-3K
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