Role of c-Jun N-terminal kinase in the PDGF-induced proliferation and migration of human adipose tissue-derived mesenchymal stem cells

Authors

  • Yong Jung Kang,

    1. Department of Physiology, Medical Research Institute, College of Medicine, Pusan National University, Busan 602-739, Republic of Korea
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  • Eun Su Jeon,

    1. Department of Physiology, Medical Research Institute, College of Medicine, Pusan National University, Busan 602-739, Republic of Korea
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  • Hae Young Song,

    1. Department of Physiology, Medical Research Institute, College of Medicine, Pusan National University, Busan 602-739, Republic of Korea
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  • Jae Suk Woo,

    1. Department of Physiology, Medical Research Institute, College of Medicine, Pusan National University, Busan 602-739, Republic of Korea
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  • Jin Sup Jung,

    1. Department of Physiology, Medical Research Institute, College of Medicine, Pusan National University, Busan 602-739, Republic of Korea
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  • Yong Keun Kim,

    1. Department of Physiology, Medical Research Institute, College of Medicine, Pusan National University, Busan 602-739, Republic of Korea
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  • Jae Ho Kim

    Corresponding author
    1. Department of Physiology, Medical Research Institute, College of Medicine, Pusan National University, Busan 602-739, Republic of Korea
    • Department of Physiology, College of Medicine, Pusan National University, 1-Ga, Ami-Dong, Suh-Gu, Busan 602-739, Republic of Korea.
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Abstract

Platelet-derived growth factor (PDGF) is a critical regulator of proliferation and migration for mesenchymal type cells. In this study, we examined the role of mitogen-activated protein (MAP) kinases in the PDGF-BB-induced proliferation and migration of human adipose tissue-derived mesenchymal stem cells (hATSCs). The PDGF-induced proliferation was prevented by a pretreatment with the c-Jun N-terminal kinase (JNK) inhibitor, SP600125. However, it was not prevented by a pretreatment with a p38 MAP kinase inhibitor, SB202190, and a specific inhibitor of the upstream kinase of extracellular signal-regulated kinase (ERK1/2), U0126. Treatment with PDGF induced the activation of JNK and ERK in hATSCs, and pretreatment with SP600125 specifically inhibited the PDGF-induced activation of JNK. Treatment with PDGF induced the cell cycle transition from the G0/G1 phase to the S phase, the elevated expression of cyclin D1, and the phosphorylation of Rb, which were prevented by a pretreatment with SP600125. In addition, the PDGF-induced migration of hATSCs was completely blocked by a pretreatment with SP600125, but not with U0126 and SB202190. These results suggest that JNK protein kinase plays a key role in the PDGF-induced proliferation and migration of mesenchymal stem cells. © 2005 Wiley-Liss, Inc.

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