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Molecular Pharmacology

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Research ArticleArticle

AMP-Activated Protein Kinase Mediates the Antiplatelet Effects of the Thiazolidinediones Rosiglitazone and Pioglitazone

Yingqiu Liu, Jung-Min Park, Kyung-Hwa Chang, Hee Jin Huh, Kyeong Lee and Moo-Yeol Lee
Molecular Pharmacology February 2016, 89 (2) 313-321; DOI: https://doi.org/10.1124/mol.115.102004
Yingqiu Liu
College of Pharmacy, (Y.L., J.M.P., K.H.C., K.L., M.Y.L.), and Department of Laboratory Medicine, Dongguk University Ilsan Hospital (H.J.H.), Dongguk University, Seoul, South Korea
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Jung-Min Park
College of Pharmacy, (Y.L., J.M.P., K.H.C., K.L., M.Y.L.), and Department of Laboratory Medicine, Dongguk University Ilsan Hospital (H.J.H.), Dongguk University, Seoul, South Korea
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Kyung-Hwa Chang
College of Pharmacy, (Y.L., J.M.P., K.H.C., K.L., M.Y.L.), and Department of Laboratory Medicine, Dongguk University Ilsan Hospital (H.J.H.), Dongguk University, Seoul, South Korea
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Hee Jin Huh
College of Pharmacy, (Y.L., J.M.P., K.H.C., K.L., M.Y.L.), and Department of Laboratory Medicine, Dongguk University Ilsan Hospital (H.J.H.), Dongguk University, Seoul, South Korea
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Kyeong Lee
College of Pharmacy, (Y.L., J.M.P., K.H.C., K.L., M.Y.L.), and Department of Laboratory Medicine, Dongguk University Ilsan Hospital (H.J.H.), Dongguk University, Seoul, South Korea
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Moo-Yeol Lee
College of Pharmacy, (Y.L., J.M.P., K.H.C., K.L., M.Y.L.), and Department of Laboratory Medicine, Dongguk University Ilsan Hospital (H.J.H.), Dongguk University, Seoul, South Korea
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Abstract

The thiazolidinedione antidiabetic drugs rosiglitazone and pioglitazone exert antiplatelet effects. Such effects are known to be mediated by the peroxisome proliferator-activated receptor γ (PPARγ), an acknowledged target of the thiazolidinediones, although the molecular mechanism is elusive. Recently, AMP-activated protein kinase (AMPK) signaling was reported to inhibit platelet aggregation. Because AMPK is another target of the thiazolidinediones, the impact of rosiglitazone and pioglitazone on platelet AMPK and its involvement in aggregation were investigated to assess the contribution of AMPK to the antiplatelet activity of these agents. Treatment with rosiglitazone stimulated both AMPK and PPARγ in isolated rat platelets. However, the concentration and the treatment time required for activation were distinct from each other. Indeed, stimulation of AMPK and PPARγ were discrete events without any cross-activation in platelets. Activation of AMPK or PPARγ by rosiglitazone rendered platelets less responsive to aggregatory stimuli such as collagen, ADP, and thrombin. However, the resultant efficacy caused by activating AMPK was higher than that attributable to PPARγ stimulation. Similar results were obtained with pioglitazone. Taken together, rosiglitazone and pioglitazone inhibit platelet aggregation by activating AMPK. AMPK functions as a potential target of rosiglitazone and pioglitazone for their antiplatelet activity, although the in vivo or clinical relevance remains to be assessed.

Footnotes

    • Received October 10, 2015.
    • Accepted November 23, 2015.
  • This research was supported by the Basic Science Research Program [NRF-2010-0008992] and the Bio & Medical Technology Development Program [2012M3A9C1053532] of the National Research Foundation (NRF) funded by the Ministry of Education and the Ministry of Science, ICT & Future Planning.

  • dx.doi.org/10.1124/mol.115.102004.

  • ↵Embedded ImageThis article has supplemental material available at molpharm.aspetjournals.org.

  • Copyright © 2016 by The American Society for Pharmacology and Experimental Therapeutics
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Molecular Pharmacology: 89 (2)
Molecular Pharmacology
Vol. 89, Issue 2
1 Feb 2016
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Research ArticleArticle

Antiplatelet Effects of Thiazolidinediones

Yingqiu Liu, Jung-Min Park, Kyung-Hwa Chang, Hee Jin Huh, Kyeong Lee and Moo-Yeol Lee
Molecular Pharmacology February 1, 2016, 89 (2) 313-321; DOI: https://doi.org/10.1124/mol.115.102004

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Research ArticleArticle

Antiplatelet Effects of Thiazolidinediones

Yingqiu Liu, Jung-Min Park, Kyung-Hwa Chang, Hee Jin Huh, Kyeong Lee and Moo-Yeol Lee
Molecular Pharmacology February 1, 2016, 89 (2) 313-321; DOI: https://doi.org/10.1124/mol.115.102004
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