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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Restoration of gap junctional intercellular communication by dibutyryl-cAMP in renal epithelial cells treated with renal carcinogen.

Dimethylnitrosamine(DMN) is an alkylating agent and a known renal carcinogen. A short exposure of renal epithelial cells to cytotoxic concentrations of DMN influences the expression of gap junction proteins. In this study, we examined gap junctional intercellular communication and connexin 43 expression in renal epithelial cells treated with 1% DMN and also examined the effects of dibutyryl-cAMP on preventing gap junctional disturbances. Connexin 43 becomes hypophosphorylated after treatment with 1% DMN for 15 minutes, but this hypophosphorylation is inhibited by pretreatment with dibutyryl-cAMP. These results suggest that changes in gap junction protein expression are early events associated with 1% DMN treatment of renal epithelial cells, and such changes are prevented by dibutyryl-cAMP pretreatment.[1]

References

  1. Restoration of gap junctional intercellular communication by dibutyryl-cAMP in renal epithelial cells treated with renal carcinogen. Sato, H., Nomata, K., Noguchi, M., Takahashi, H., Watanabe, J., Kanetake, H. Anticancer Res. (2003) [Pubmed]
 
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