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role of macrophage migration inhibitory factor in the proliferation of smooth muscle cell in pulmonary hypertension巨噬细胞迁移抑制因子的作用在肺动脉高压的平滑肌细胞的增殖.pdf

role of macrophage migration inhibitory factor in the proliferation of smooth muscle cell in pulmonary hypertension巨噬细胞迁移抑制因子的作用在肺动脉高压的平滑肌细胞的增殖.pdf

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role of macrophage migration inhibitory factor in the proliferation of smooth muscle cell in pulmonary hypertension巨噬细胞迁移抑制因子的作用在肺动脉高压的平滑肌细胞的增殖

Hindawi Publishing Corporation Mediators of Inflammation Volume 2012, Article ID 840737, 10 pages doi:10.1155/2012/840737 Research Article Role of Macrophage Migration Inhibitory Factor in the Proliferation of Smooth Muscle Cell in Pulmonary Hypertension Bo Zhang,1, 2 Min Shen,3 Min Xu,1, 2 Li-Li Liu,4 Ying Luo,1, 2 Dun-Quan Xu,1, 2 Yan-Xia Wang,1, 2 Man-Ling Liu,1, 2 Yi Liu,1, 2 Hai-Ying Dong,1, 2 Peng-Tao Zhao,1, 2 and Zhi-Chao Li1, 2 1 Department of Pathology, Xijing Hospital, Fourth Military Medical University, Changle West Road 169, Xi’an 710032, China 2 Department of Pathology and Pathophysiology, Fourth Military Medical University, Xi’an 710032, China 3 Department of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, China 4 Department of Oncology, Tangdu Hospital, Fourth Military Medical University, Xi’an 710032, China Correspondence should be addressed to Zhi-Chao Li, lizhic@ Received 14 June 2011; Accepted 11 October 2011 Academic Editor: Dennis Daniel Taub Copyright © 2012 Bo Zhang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Pulmonary hypertension (PH) contributes to the mortality of patients with lung and heart diseases. However, the underlying mechanism has not been completely elucidated. Accumulating evidence suggests that inflammatory response may be involved in the pathogenesis of PH. Macrophage migration inhibitory factor (MIF) is a critical upstream inflammatory mediator which promotes a broad range of pathophysiological processes. The aim of the study was to investigate the role of MIF in the pulmonary vascular remodeling of hypoxia-induc

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