J. Lipid Res.
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A more recent version of this article appeared on March 1, 2006

Papers In Press, published online ahead of print December 7, 2005
J. Lipid Res., doi:10.1194/jlr.M500508-JLR200
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Submitted on November 21, 2005
Accepted on December 7, 2005

Sphingosylphosphorylcholine induces proliferation of human adipose tissue-derived mesenchymal stem cells via activation of JNK

Eun Su Jeon, Hae Young Song, Mi Ra Kim, Hyun Jung Moon, Yong Chan Bae, Jin Sup Jung, and Jae Ho Kim

Dept. of Physiology, Pusan National University, College of Medicine, Busan 602-739

Corresponding Author: jhkimst{at}pusan.ac.kr

Sphingosylphosphorylcholine (SPC) has been implicated in a variety of cellular responses, including proliferation and differentiation. In the present study, we demonstrated that D-erythro-, but not L-threo-SPC, stereo-selectively stimulated the proliferation of human adipose tissue-derived mesenchymal stem cells (hADSCs) with a maximal increase at 5 mu M and increased the intracellular concentration of Ca2+ ([Ca2+]i) in hADSCs, which do not express known SPC receptors, i.e. OGR1, GPR4, G2A, and GPR12. The SPC-induced proliferation and increase in [Ca2+]i were sensitive to pertussis toxin (PTX) and phospholipase C (PLC) inhibitor U73122, suggesting that PTX-sensitve G proteins, Gi or Go, and PLC are involved in the SPC-induced proliferation. In addition, SPC treatment induced the phosphorylation of c-Jun and ERK, and the SPC-induced proliferation was completely prevented by pretreatment with Jun N-terminal kinase (JNK)-specific inhibitor SP600125, but not with MEK-specific inhibitor U0126. Furthermore, the SPC-induced proliferation and JNK activation were completely attenuated by over-expression of a dominant negative mutant of JNK2, and the SPC-induced activation of JNK was inhibited by pretreatment with PTX or U73122. Treatment of hADSCs with LPA receptor antagonist, Ki16425, had no impact on the SPC-induced increase in [Ca2+]i. However, the SPC-induced proliferation was partially, but significantly, attenuated by pretreatment of the cells with Ki16425. These results indicate that SPC stimulates proliferation of hADSCs through Gi/o-PLC-JNK pathway, and that LPA receptors may be responsible in part for the SPC-induced proliferation.


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