scholarly journals Role of Macrophage Migration Inhibitory Factor in the Proliferation of Smooth Muscle Cell in Pulmonary Hypertension

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Bo Zhang ◽  
Min Shen ◽  
Min Xu ◽  
Li-Li Liu ◽  
Ying Luo ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Heart Diseases ◽  
Pulmonary Arteries ◽  
Underlying Mechanism ◽  
Inhibitory Factor ◽  
Macrophage Migration

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-induced PH. We found that MIF mRNA and protein expression was increased in the lung tissues from hypoxic pulmonary hypertensive rats. Intensive immunoreactivity for MIF was observed in smooth muscle cells of large pulmonary arteries (PAs), endothelial cells of small PAs, and inflammatory cells of hypoxic lungs. MIF participated in the hypoxia-induced PASMCs proliferation, and it could directly stimulate proliferation of these cells. MIF-induced enhanced growth of PASMCs was attenuated by MEK and JNK inhibitor. Besides, MIF antagonist ISO-1 suppressed the ERK1/2 and JNK phosphorylation induced by MIF. In conclusion, the current finding suggested that MIF may act on the proliferation of PASMCs through the activation of the ERK1/2 and JNK pathways, which contributes to hypoxic pulmonary hypertension.

scholarly journals Multiple roles of macrophage migration inhibitory factor in pulmonary hypertension

2020 ◽  
Vol 318 (1) ◽  
pp. L1-L9 ◽  
Author(s):  
Gael Jalce ◽  
Christophe Guignabert
Keyword(s):  
Pulmonary Hypertension ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Scientific Evidence ◽  
Pulmonary Arteries ◽  
Inhibitory Factor ◽  
Pulmonary Vasculature ◽  
Macrophage Migration ◽  
Multifactorial Diseases ◽  
Pulmonary Arterial

Pulmonary hypertension (PH) is a life-threatening condition arising from the loss and obstructive remodeling of the pulmonary arteries, leading to the sustained elevation of pulmonary arterial pressure (PAP) and pulmonary vascular resistance (PVR) and subsequently right ventricular (RV) failure and death. PH encompasses a group of multifactorial diseases, such as pulmonary arterial hypertension (PAH) and chronic thromboembolic PH, for which there is no treatment that can stop or reverse the progression of remodeling of the pulmonary vasculature. The identification of new molecular targets for the development of more effective drugs is thus urgently needed. In this context, macrophage migration inhibitory factor (MIF), a pleiotropic upstream proinflammatory mediator, is emerging as a promising molecular target, as it contributes to perivascular inflammation and pulmonary arterial remodeling, two key hallmarks of PAH that are not specifically targeted by currently approved therapies. The objective of this review is to summarize the scientific evidence on the pathogenic roles of MIF and its potential as a biomarker and therapeutic target in PH/PAH.

scholarly journals Role of Macrophage Migration Inhibitory Factor in the Regulatory T Cell Response of Tumor-Bearing Mice

2012 ◽  
Vol 189 (8) ◽  
pp. 3905-3913 ◽  
Author(s):  
Susanna Choi ◽  
Hang-Rae Kim ◽  
Lin Leng ◽  
Insoo Kang ◽  
William L. Jorgensen ◽  
...  
Keyword(s):  
T Cell ◽  
Migration Inhibitory Factor ◽  
Regulatory T Cell ◽  
Cell Response ◽  
Macrophage Migration Inhibitory Factor ◽  
T Cell Response ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Tumor Bearing

scholarly journals The role of human macrophage migration inhibitory factor in promoting angiogenesis

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
XiYong Yu ◽  
ZhiXin Shan ◽  
QiuXiong Lin ◽  
ShiXia Cai ◽  
Min Yang ◽  
...  
Keyword(s):  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Human Macrophage ◽  
Macrophage Migration

Role of macrophage migration inhibitory factor in bleomycin-induced lung injury and fibrosis in mice

2002 ◽  
Vol 283 (1) ◽  
pp. L156-L162 ◽  
Author(s):  
Yoshinori Tanino ◽  
Hironi Makita ◽  
Kenji Miyamoto ◽  
Tomoko Betsuyaku ◽  
Yoshinori Ohtsuka ◽  
...  
Keyword(s):  
Lung Injury ◽  
Migration Inhibitory Factor ◽  
Lung Fibrosis ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Lung Injury Score ◽  
Macrophage Migration ◽  
Acute Lung Inflammation ◽  
Intratracheal Administration

Macrophage migration inhibitory factor (MIF) is a unique cytokine that reportedly overrides the anti-inflammatory effect of endogenous glucocorticoids. MIF has been demonstrated to be involved in a variety of inflammatory diseases. In this study, we examined the role of MIF in bleomycin (BLM)-induced lung injury and fibrosis. The levels of MIF in lung tissues and bronchoalveolar lavage fluids were significantly increased in the period 5–10 days after intratracheal administration of BLM. Treatment with the anti-MIF antibody significantly reduced the mortality at 14 days and the histopathological lung injury score at 10 days. These effects were accompanied with significant suppression of the accumulation of inflammatory cells in the alveolar space and tumor necrosis factor-α in the lungs at 7 days. However, the anti-MIF antibody did not affect either the content of lung hydroxyproline or the histopathological lung fibrosis score at 21 days after BLM. These data provide further evidence for the crucial role of MIF in acute lung inflammation but do not support the involvement of MIF in lung fibrosis induced by BLM in mice.

Sign in / Sign up

Export Citation Format

Share Document