Role of Macrophage Migration Inhibitory Factor in the Proliferation of Smooth Muscle Cell in Pulmonary Hypertension
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 inhibitor...
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| Main Authors: | , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
2012-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2012/840737 |
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| Summary: | 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. |
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| ISSN: | 0962-9351 1466-1861 |