Oncostatin M promotes osteogenesis and suppresses adipogenic differentiation of human adipose tissue-derived mesenchymal stem cells

Authors

  • Hae Young Song,

    1. Research Center for Ischemic Tissue Regeneration & Medical Research Institute, Pusan National University, Busan 602-739, Republic of Korea
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  • Eun Su Jeon,

    1. Research Center for Ischemic Tissue Regeneration & Medical Research Institute, Pusan National University, Busan 602-739, Republic of Korea
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  • Jung Il Kim,

    1. Department of Orthopaedic Surgery, College of Medicine, Pusan National University, Busan 602-739, Republic of Korea
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  • Jin Sup Jung,

    1. Research Center for Ischemic Tissue Regeneration & Medical Research Institute, Pusan National University, Busan 602-739, Republic of Korea
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  • Jae Ho Kim

    Corresponding author
    1. Research Center for Ischemic Tissue Regeneration & Medical Research Institute, 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

Oncostatin M (OSM) is a multifunctional cytokine of the interleukin-6 family and has been implicated in embryonic development, differentiation, inflammation, and regeneration of liver and bone. In the present study, we demonstrated that treatment of human adipose mesenchymal stem cells (hADSCs) with OSM-attenuated adipogenic differentiation, as indicated by decreased accumulation of intracellular lipid droplets and down-regulated expression of adipocytic markers, such as lipoprotein lipase and PPARγ. However, OSM treatment stimulated osteogenic differentiation, as demonstrated by the increase in matrix mineralization and expression levels of osteogenic differentiation markers, including alkaline phosphatase, Runx2, and osteocalcin. OSM treatment induced activation of JAK2, JAK3, and ERK in hADSCs, and pre-treatment of hADSCs with the JAK2 inhibitor, AG490, significantly restored the OSM-induced inhibition of adipogenic differentiation. Whereas, the JAK3 inhibitor, WHI-P131, and the MEK inhibitor, U0126, had no effects on the anti-adipogenic activity of OSM. On the other hand, the pro-osteogenic activity of OSM was prevented by treatment of the cells with WHI-P131 or U0126, but not with AG490. These results indicate that distinct signaling pathways, including JAK2, JAK3, and MEK-ERK, play specific roles in the OSM-induced anti-adipogenic and pro-osteogenic differentiation of hADSCs. J. Cell. Biochem. 101:1238–1251, 2007. © 2007 Wiley-Liss, Inc.

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