Enhancement of gap junctional intercellular communication by dibutyryl cyclic AMP in lung epithelial cells.
Reduced gap junctional intercellular communication (GJIC) occurs in neoplastic cells and contributes to their phenotype. Cyclic AMP agonists inhibit lung cancer cell growth and enhance GIIC in other cell types, but little is known about their effects on lung epithelial cell gap junctions. We have examined whether N6, 2'-O-dibutyryladenosine 3':5'-cyclic mono-phosphate (DBcAMP) affected GJIC, gap junction protein (connexin43) expression, and the growth of non-transformed and neoplastic mouse lung epithelial cells. DBcAMP (0.01.1 mM) stimulated GJIC (assayed by fluorescent dye microinjection) and connexin43 expression (assessed by Northern and Western blotting) and reduced their proliferation. These results suggest an association between cAMP growth inhibition and enhanced GJIC in lung epithelial cells.
Banoub
R W
RW
Department of Pathology, Medical College of Ohio, Toledo 43699, USA.
Fernstrom
M
M
Malkinson
A M
AM
Ruch
R J
RJ
D000818:Animals; D003994:Bucladesine / Q000494:pharmacology*; D002450:Cell Communication / Q000187:drug effects*; D018031:Connexin 43 / Q000378:metabolism; D004848:Epithelium / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure; D017629:Gap Junctions / Q000187:drug effects*; D008168:Lung / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D051379:Mice; D010766:Phosphorylation
D018031:Connexin 43; D003994:Bucladesine