Central South University, Changsha, China
Copyright 2016, American College of Chest Physicians. All Rights Reserved.
SESSION TITLE: Diffuse Lung Disease: Interstitial Lung Disease
SESSION TYPE: Original Investigation Poster
PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM
PURPOSE: Pulmonary fibrosis is a sever disease which threaten human health, with progressing myofibroblast proliferation, extracellular matrix accumulation. Epithelial-mesenchymal transition (EMT) is an important resource of myofibroblast in pulmonary fibrosis. We had found that NMDA receptors participated in bleomycin induced acute lung injury. We aimed to find out whether NMDA receptors activation contributes to EMT.
METHODS: MLE-12 cells are divided into teo groups: Con, NMDA and harvested 48h after NMDA or TGFβ1 stimulation. Mesenchymal cell marker α-SMA and alveolar epithelial cell markers SP-C, E-cadherin expression and phosphorylation of MAPK signal pathway were detected by Real-time qPCR and/or western blot.
RESULTS: NMDA receptors were expressed on MLE-12, mice alveolar epithelial cell line by RT-PCR and western blot. After 10mM NMDA stimulation α-SMA mRNA expression (P<0.01) and protein expression trend were increased, the trend of SP-C mRNA expression were decreased (P=0.1) and E-Cadherin protein expression were decreased (P<0.05) in MLE-12. The phosphorylation levels of MAPKs were increased, including ERK, JNK, p38 protein.
CONCLUSIONS: 10mM NMDA can induce EMT and MAPKs phosphorylation in MLE-12. NMDA receptors activation promote EMT may be involved in MAPKs phosphorylation.
CLINICAL IMPLICATIONS: NMDA receptors may play an important role in treatment of pulmonary fibrosis.
DISCLOSURE: The following authors have nothing to disclose: Yang Li, Fei-Yan Zhao, Wei Liu, Yan-Hong Huang, Chen Li, Dan-Dan Feng, Jian-Zhong Han, Zi-Qiang Luo
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