Development of mucous cells in mouse intrapulmonary airways induced by cholera toxin, dibutyryl cyclic AMP and prostaglandin E1.
The effect of cholera toxin (CT), dibutyryl cyclic adenosinemonophosphate (DE-cAMP) and prostaglandin E1 (PGE1) on the morphological appearance of mouse intrapulmonary airway epithelium has been studied. All three secretagogues, known to mediate their activity via cAMP, induced increased numbers of mucous cells, but with different kinetics. After exposure to DB-cAMP, mucous cells appeared after 7 h with a peak value at 48 h. The corresponding values for PGE1 were 24 h for the appearance and 48 h for peak value whereas exposure to CT gave a lower response with a peak at 72 h. Autoradiography of lungs from mice injected with 3H-thymidine showed that the mucous cells appeared without any foregoing DNA synthesis, however, increased numbers of labelled cells were seen as a late response to the secretagogues.
D000262:Adenylyl Cyclases / Q000378:metabolism; D000527:Alprostadil; D000818:Animals; D003994:Bucladesine / Q000494:pharmacology*; D002772:Cholera Toxin / Q000494:pharmacology*; D008168:Lung / Q000187:drug effects* / Q000201:enzymology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008938:Mitosis / Q000187:drug effects; D009093:Mucus / Q000166:cytology / Q000187:drug effects*; D011458:Prostaglandins E / Q000494:pharmacology*; D013997:Time Factors; D014132:Trachea / Q000187:drug effects*
D011458:Prostaglandins E; D003994:Bucladesine; D002772:Cholera Toxin; D000262:Adenylyl Cyclases; D000527:Alprostadil