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. 1996 Apr;57(2):81-90.
doi: 10.1006/bmme.1996.0013.

The role of calcium in the artificially induced decidual cell reaction in pseudopregnant mice

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The role of calcium in the artificially induced decidual cell reaction in pseudopregnant mice

J A Sakoff et al. Biochem Mol Med. 1996 Apr.

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.

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