PMID- 12855408
OWN - NLM
STAT- MEDLINE
DCOM- 20040413
LR  - 20071114
IS  - 1044-1549 (Print)
IS  - 1044-1549 (Linking)
VI  - 30
IP  - 2
DP  - 2004 Feb
TI  - Ionotropic glutamate receptors in lungs and airways: molecular basis for 
      glutamate toxicity.
PG  - 139-44
AB  - We earlier showed that the ionotropic glutamate receptor agonist N-methyl 
      D-aspartate (NMDA) induces excitotoxic pulmonary edema, and that endogenous 
      activation of NMDA receptors (NMDAR) could mediate lung injury caused by 
      oxidative stress. In this study, we searched for evidence of NMDAR expression in 
      the rat lung and in the alveolar macrophage (AM) cell line NR8383, and for 
      possible regulation of receptor expression by NMDA. The presence of mRNA for 
      NMDAR 1 and the four known NMDAR 2 subtypes (A, B, C, and D) was examined by 
      reverse transcriptase-polymerase chain reaction using isoform-specific primers. 
      NMDAR 1 was expressed in all lung regions examined (peripheral, midlung, and 
      mainstem), as well as in trachea and the AMs. Expression of NMDAR 2A and 2B 
      subtypes was not detected, whereas NMDAR 2C was present only in peripheral and 
      mid-lung samples. NMDAR 2D was the dominant subtype expressed in the peripheral, 
      gas-exchange zone of lung and in alveolar macrophages, and this expression was 
      upregulated in lungs treated with NMDA. Western blot confirmed the presence of 
      NMDAR 1 protein in all lung regions and in AMs. These findings provide a 
      molecular-biological basis for the excitotoxic actions of glutamate in rat lungs 
      and airways, and raise the question of a possible physiologic role for NMDAR in 
      lung and airway function.
FAU - Dickman, Kathleen G
AU  - Dickman KG
AD  - V.A. Medical Center, Northport, NY, USA.
FAU - Youssef, J Georges
AU  - Youssef JG
FAU - Mathew, Suni M
AU  - Mathew SM
FAU - Said, Sami I
AU  - Said SI
LA  - eng
GR  - HL-30450/HL/NHLBI NIH HHS/United States
GR  - HL-70212/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
DEP - 20030710
PL  - United States
TA  - Am J Respir Cell Mol Biol
JT  - American journal of respiratory cell and molecular biology
JID - 8917225
RN  - 0 (Protein Isoforms)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 6384-92-5 (N-Methylaspartate)
SB  - IM
MH  - Animals
MH  - Cell Line
MH  - Lung/*anatomy & histology/*metabolism
MH  - Macrophages, Alveolar/cytology/metabolism
MH  - Male
MH  - N-Methylaspartate/metabolism
MH  - Protein Isoforms/genetics/metabolism
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, N-Methyl-D-Aspartate/genetics/*metabolism
EDAT- 2003/07/12 05:00
MHDA- 2004/04/14 05:00
CRDT- 2003/07/12 05:00
PHST- 2003/07/12 05:00 [pubmed]
PHST- 2004/04/14 05:00 [medline]
PHST- 2003/07/12 05:00 [entrez]
AID - 2003-0177OC [pii]
AID - 10.1165/rcmb.2003-0177OC [doi]
PST - ppublish
SO  - Am J Respir Cell Mol Biol. 2004 Feb;30(2):139-44. doi: 10.1165/rcmb.2003-0177OC. 
      Epub 2003 Jul 10.