title: The role of calcium in the artificially induced decidual cell reaction in pseudopregnant mice.
abstract: The present study was designed to test the hypothesis that Ca2+ is required for the successful induction of the decidual cell reaction (DCR) in mice following stimulation with concanavalin A (Con A). Con A (125 micrograms) administered intraluminally on Day 4 of pseudopregnancy increased uterine vascular permeability increased uterine weight, and induced morphological and histological transformations that were clearly indicative of decidualization. Radioactive CaCl2 (1 mmol liter-1, 600 mCi mmol-1 introduced into the uterine lumen with either Con A or saline was subsequently incorporated into the uterine tissue and detected only in the luminal epithelium by microautoradiography techniques. The intraluminal administration of CaCl2 in combination with Con A increased the magnitude of the lectin-induced DCR. In contrast, the administration of other cationic chloride solutions, at various concentrations and tonicity, either had no effect (viz. Na+, Mg2+, and Ba2+) or reduced (viz. K+, Zn2+, Cd2+, and La3+) this uterine response. While ionophore A23187 was also deciduogenic, it suppressed the DCR when administered before Con A and enhanced the DCR when administered after Con A. The Ca2+ channel blockers, nifedipine, verapamil, nicardipine, and diltiazem, the Ca(2+)-calmodulin inhibitor, W7, and the Ca(+)-ATPase inhibitor, thapsigargin also effectively reduced the uterine response to Con A when administered intraluminally. However, the Con A A-induced DCR was not influenced by the Ca+ chelators, EGTA, EDTA, BAPTA, and BAPTA-AM. The results confirm that Con A is deciduogenic in pseudopregnant mice and suggest that luminal Ca2+ plays an important role in facilitating the induction of the lectin-induced DCR by influencing the metabolism of the luminal epithelium.
authors: Department of Biological Sciences, University of Newcastle, Callaghan N.S.W, Australia.
authors: J A
authors: JA
authors: Sakoff
authors: R N
authors: RN
authors: Murdoch
mesh_terms: D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002132:Calcium Radioisotopes; D000252:Calcium-Transporting ATPases / Q000037:antagonists & inhibitors; D002413:Cations, Divalent / Q000494:pharmacology; D003208:Concanavalin A / Q000494:pharmacology; D003656:Decidua / Q000187:drug effects / Q000502:physiology*; D004492:Edetic Acid / Q000494:pharmacology; D004533:Egtazic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D051379:Mice; D008817:Mice, Mutant Strains; D011555:Pseudopregnancy; D019284:Thapsigargin / Q000494:pharmacology; D014599:Uterus / Q000187:drug effects / Q000502:physiology
chemical_list: D002121:Calcium Channel Blockers; D002132:Calcium Radioisotopes; D002413:Cations, Divalent; D004791:Enzyme Inhibitors; D003208:Concanavalin A; C070379:1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester; D000001:Calcimycin; D004533:Egtazic Acid; D019284:Thapsigargin; D004492:Edetic Acid; D000252:Calcium-Transporting ATPases; C025603:1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid; D002118:Calcium