Modification of gap junctional intercellular communication by changes in extracellular pH in Syrian hamster embryo cells

1990 ◽  
Vol 11 (6) ◽  
pp. 909-913 ◽  
Author(s):  
Randall J. Ruch ◽  
James E. Klaunig ◽  
James E. Klaunig ◽  
Gary A. Kerckaert ◽  
Robert A. LeBoeuf ◽  
...  
1992 ◽  
Vol 20 (2) ◽  
pp. 213-217
Author(s):  
Svein-Ole Mikalsen ◽  
Edgar Rivedal ◽  
Tore Sanner

The effects of NiSO4, K2CrO4, PbAc2, CrCl3 and CdAc2 on gap junctional intercellular communication (GJIC) were studied. Two exposure procedures were used — A: an established monolayer of cells was exposed to the compound, and B: the compound was mixed with the cells before seeding. The apparent inhibition of GJIC by CrCl3 and CdAc2 could be accounted for by cytotoxicity, i.e. disruption of physical contacts between cells. PbAc2 had no effect on GJIC. The effects of NiSO4 and K2CrO4 depended on the exposure procedure and cell type studied. Specifically, K2CrO4 induced a significant increase in GJIC in BPNi cells by procedure A, and a decrease by procedure B. The cytotoxic effects of NiSO4 were examined in more detail. The toxic concentrations varied widely between the methods used. The results indicate that the effect of compounds on GJIC may vary with different exposure procedures, and that inhibition of GJIC is not due to general cytotoxic effects.


2014 ◽  
Vol 307 (1) ◽  
pp. G24-G32 ◽  
Author(s):  
Anamika M. Reed ◽  
Thomas Kolodecik ◽  
Sohail Z. Husain ◽  
Fred S. Gorelick

Decreased extracellular pH is observed in a number of clinical conditions and can sensitize to the development and worsen the severity of acute pancreatitis. Because intercellular communication through gap junctions is pH-sensitive and modulates pancreatitis responses, we evaluated the effects of low pH on gap junctions in the rat pancreatic acinar cell. Decreasing extracellular pH from 7.4 to 7.0 significantly inhibited gap junctional intracellular communication. Acidic pH also significantly reduced levels of connexin32, the predominant gap junction protein in acinar cells, and altered its localization. Increased degradation through the proteasomal, lysosomal, and autophagic pathways mediated the decrease in connexin32 under low-pH conditions. These findings provide the first evidence that low extracellular pH can regulate gap junctional intercellular communication by enhancing connexin degradation.


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