Abstract:
:N-methyl-D-aspartate (NMDA) receptors are ionotropic glutamate receptors widely distributed in the central nervous system, and have been extensively investigated for their roles in embryonic development, synaptic plasticity and neuroexcitoxicity. Their functions in the peripheral nervous system and non-neural tissues have caught much attention recently. Over-activation of NMDA receptors induces excitotoxic lung injury. But the endogenous cell types in the lungs that express NMDA receptors remains elusive and the molecular mechanism underlies NMDA-induced lung injury has not been fully characterized. In this work, we reported that functional NMDA receptors were expressed in alveolar type II cells in the lungs. Over-activation of these receptors led to down-regulation of pulmonary surfactants synthesis. We further demonstrated that decreased cellular choline-phosphate cytidylyltransferase alpha expression induced by NMDA treatment accounted for the decreased pulmonary surfactants synthesis. Our results provided important clues for treatment of glutamate lung injury by modulating pulmonary surfactants system.
journal_name
Basic Clin Pharmacol Toxicoljournal_title
Basic & clinical pharmacology & toxicologyauthors
Shen L,Li L,She H,Yue S,Li C,Luo Zdoi
10.1111/j.1742-7843.2010.00572.xsubject
Has Abstractpub_date
2010-09-01 00:00:00pages
751-7issue
3eissn
1742-7835issn
1742-7843pii
PTO572journal_volume
107pub_type
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