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Role of c‐Jun N‐terminal kinase in the PDGF‐induced proliferation and migration of human adipose tissue‐derived mesenchymal stem cells
Author(s) -
Kang Yong Jung,
Jeon Eun Su,
Song Hae Young,
Woo Jae Suk,
Jung Jin Sup,
Kim Yong Keun,
Kim Jae Ho
Publication year - 2005
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.20499
Subject(s) - platelet derived growth factor receptor , microbiology and biotechnology , mesenchymal stem cell , kinase , chemistry , cell growth , mitogen activated protein kinase , biology , growth factor , biochemistry , receptor
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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