TY - JOUR
T1 - Activation of vasculogenic progenitor cells by ent-16α,17-dihydroxy- kauran-19-oic acid
AU - Park, So Hyun
AU - Jeong, Yun Mi
AU - Kim, Ji Hye
AU - Chung, Hyung Min
AU - Suh, Wonhee
AU - Sung, Sang Hyun
AU - Park, Sang Gyu
AU - Sung, Jong Hyuk
PY - 2011/12
Y1 - 2011/12
N2 - Vasculogenic progenitor cells (VPCs) circulate in the blood and have the ability to differentiate into endothelial cells that make up the lining of blood vessels. Therefore, VPC transplantation is a new strategy for the treatment of ischemic diseases. Because priming/preconditioning of VPCs before transplantation enhances their regenerative potential, the present study investigated whether ent-16α,17-dihydroxy-kauran-19-oic acid (DHK) isolated from Siegesbeckia pubescens could stimulate/activate VPCs in vitro. Therefore, the effect of DHK (1-100 μM concentration) on the proliferation, migration, and tube forming of VPCs was examined in various systems, and related signaling pathways were identified. DHK treatment significantly increased the proliferation, migration, and tube formation of VPCs in a dose-dependent manner. Phosphorylation of extracellular signal-regulated kinase (ERK)1/2 and Akt was significantly increased by DHK, but chemical inhibitors against ERK1/2 (U0126) and Akt (LY294002) significantly attenuated DHK-enhanced proliferation, migration, and tube formation of VPCs. Collectively, these results indicated that DHK shows promise as a novel VPC primer/activator.
AB - Vasculogenic progenitor cells (VPCs) circulate in the blood and have the ability to differentiate into endothelial cells that make up the lining of blood vessels. Therefore, VPC transplantation is a new strategy for the treatment of ischemic diseases. Because priming/preconditioning of VPCs before transplantation enhances their regenerative potential, the present study investigated whether ent-16α,17-dihydroxy-kauran-19-oic acid (DHK) isolated from Siegesbeckia pubescens could stimulate/activate VPCs in vitro. Therefore, the effect of DHK (1-100 μM concentration) on the proliferation, migration, and tube forming of VPCs was examined in various systems, and related signaling pathways were identified. DHK treatment significantly increased the proliferation, migration, and tube formation of VPCs in a dose-dependent manner. Phosphorylation of extracellular signal-regulated kinase (ERK)1/2 and Akt was significantly increased by DHK, but chemical inhibitors against ERK1/2 (U0126) and Akt (LY294002) significantly attenuated DHK-enhanced proliferation, migration, and tube formation of VPCs. Collectively, these results indicated that DHK shows promise as a novel VPC primer/activator.
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U2 - 10.1248/bpb.34.1801
DO - 10.1248/bpb.34.1801
M3 - Article
C2 - 22130234
AN - SCOPUS:83255164200
SN - 0918-6158
VL - 34
SP - 1801
EP - 1807
JO - Biological and Pharmaceutical Bulletin
JF - Biological and Pharmaceutical Bulletin
IS - 12
ER -