TY - JOUR A2 - Taub, Dennis Daniel AU - Zhang, Bo AU - Shen, Min AU - Xu, Min AU - Liu, Li-Li AU - Luo, Ying AU - Xu, Dun-Quan AU - Wang, Yan-Xia AU - Liu, Man-Ling AU - Liu, Yi AU - Dong, Hai-Ying AU - Zhao, Peng-Tao AU - Li, Zhi-Chao PY - 2012 DA - 2012/01/18 TI - Role of Macrophage Migration Inhibitory Factor in the Proliferation of Smooth Muscle Cell in Pulmonary Hypertension SP - 840737 VL - 2012 AB - Pulmonary hypertension (PH) contributes to the mortality ofpatients with lung and heart diseases. However, the underlyingmechanism has not been completely elucidated. Accumulatingevidence suggests that inflammatory response may be involved inthe pathogenesis of PH. Macrophage migration inhibitory factor(MIF) is a critical upstream inflammatory mediator which promotesa broad range of pathophysiological processes. The aim of thestudy was to investigate the role of MIF in the pulmonary vascularremodeling of hypoxia-induced PH. We found that MIF mRNA andprotein expression was increased in the lung tissues from hypoxicpulmonary hypertensive rats. Intensive immunoreactivity for MIFwas observed in smooth muscle cells of large pulmonary arteries(PAs), endothelial cells of small PAs, and inflammatory cells ofhypoxic lungs. MIF participated in the hypoxia-induced PASMCsproliferation, and it could directly stimulate proliferation ofthese cells. MIF-induced enhanced growth of PASMCs was attenuatedby MEK and JNK inhibitor. Besides, MIF antagonist ISO-1 suppressedthe ERK1/2 and JNK phosphorylation induced by MIF. In conclusion,the current finding suggested that MIF may act on theproliferation of PASMCs through the activation of the ERK1/2 andJNK pathways, which contributes to hypoxic pulmonary hypertension. SN - 0962-9351 UR - https://doi.org/10.1155/2012/840737 DO - 10.1155/2012/840737 JF - Mediators of Inflammation PB - Hindawi Publishing Corporation KW - ER -