PMID- 1650375
OWN - NLM
STAT- MEDLINE
DCOM- 19910905
LR  - 20191210
IS  - 0021-9541 (Print)
IS  - 0021-9541 (Linking)
VI  - 148
IP  - 1
DP  - 1991 Jul
TI  - Modulation of Na+/K+ exchange potentiates lipopolysaccharide-induced gene 
      expression in murine peritoneal macrophages.
PG  - 96-105
AB  - The role of Na+/K+ exchange in regulating lipopolysaccharide (LPS)-mediated 
      induction of cytokine gene expression has been examined in murine peritoneal 
      macrophages. Depletion of K+ from the culture medium resulted in a three- to 
      five-fold potentiation of tumor necrosis factor-alpha (TNF alpha), KC (gro), and 
      IP-10 mRNA expression in LPS-treated macrophages. The potentiating effect was 
      apparently the result of inhibition of Na+/K+ exchange through the 
      Na+/K(+)-adenosine triphosphatase (ATPase) because ouabain-mediated inhibition of 
      Na+/K(+)-ATPase was also able to potentiate cytokine mRNA expression as much or 
      more than did K+ depletion. The effects of K+ depletion or ouabain treatment were 
      not caused by depolarization of the macrophage membrane because depolarization 
      mediated by elevating extracellular K+ levels was inhibitory to cytokine mRNA 
      expression. Depletion of Na+ by substitution with choline in the culture medium 
      also markedly potentiated LPS-induced gene expression. The Na+/H+ antiporter was 
      not, however, involved in potentiating cytokine expression because treatment of 
      macrophages with amiloride either had no effect on or was inhibitory to the 
      LPS-induced changes in mRNA levels. The potentiation of gene expression was 
      selective and was at least partially the result of increased transcriptional 
      activity of each gene. Whereas Na+ depletion and ouabain both inhibited 86Rb+ 
      uptake by macrophages, treatment with LPS had no effect either on Rb+ uptake or 
      on efflux. Thus altered Na+/K+ exchange is not a component of the primary 
      signalling pathway(s) mediating response to LPS. Nevertheless, modulation of 
      macrophage Na+/K+ exchange by agents encountered during an inflammatory response 
      may be an important determinant of the magnitude and quality of specific gene 
      expression.
FAU - Ohmori, Y
AU  - Ohmori Y
AD  - Research Institute, Cleveland Clinic Foundation, Ohio 44106.
FAU - Reynolds, E
AU  - Reynolds E
FAU - Hamilton, T A
AU  - Hamilton TA
LA  - eng
GR  - CA 39621/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (Carrier Proteins)
RN  - 0 (Chemokine CXCL1)
RN  - 0 (Chemokine CXCL10)
RN  - 0 (Chemokines, CXC)
RN  - 0 (Cxcl1 protein, mouse)
RN  - 0 (Cytokines)
RN  - 0 (Growth Substances)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Messenger)
RN  - 0 (Rubidium Radioisotopes)
RN  - 0 (Sodium-Hydrogen Exchangers)
RN  - 0 (Sodium-Potassium-Chloride Symporters)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 5ACL011P69 (Ouabain)
RN  - EC 7.2.2.13 (Sodium-Potassium-Exchanging ATPase)
SB  - IM
MH  - Animals
MH  - Carrier Proteins/*physiology
MH  - Cells, Cultured
MH  - Chemokine CXCL1
MH  - Chemokine CXCL10
MH  - *Chemokines, CXC
MH  - Cytokines/genetics/metabolism
MH  - Gene Expression/*drug effects/physiology
MH  - Growth Substances/genetics/metabolism
MH  - *Intercellular Signaling Peptides and Proteins
MH  - Lipopolysaccharides/*pharmacology
MH  - Macrophages/drug effects/metabolism/*physiology
MH  - Mice
MH  - Mice, Inbred C3H
MH  - Mice, Inbred C57BL
MH  - Ouabain/pharmacology
MH  - RNA, Messenger/genetics/metabolism
MH  - Rubidium Radioisotopes/pharmacokinetics
MH  - Sodium-Hydrogen Exchangers
MH  - Sodium-Potassium-Chloride Symporters
MH  - Sodium-Potassium-Exchanging ATPase/physiology
MH  - Time Factors
MH  - Transcription, Genetic/drug effects/physiology
MH  - Tumor Necrosis Factor-alpha/genetics/metabolism
EDAT- 1991/07/01 00:00
MHDA- 1991/07/01 00:01
CRDT- 1991/07/01 00:00
PHST- 1991/07/01 00:00 [pubmed]
PHST- 1991/07/01 00:01 [medline]
PHST- 1991/07/01 00:00 [entrez]
AID - 10.1002/jcp.1041480112 [doi]
PST - ppublish
SO  - J Cell Physiol. 1991 Jul;148(1):96-105. doi: 10.1002/jcp.1041480112.