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Alterations in uterine calcium ions during induction of the decidual cell reaction in pseudopregnant mice

The present study exploited the deciduogenic actions of concanavalin A (Con A) in pseudopregnant Quackenbush strain mice to assess whether alterations in uterine Ca²⁺ status accompany stromal cell transformations that culminate in the decidual cell reaction and the establishment of pregnancy. It was found that the introduction of 15 blastocyst-size Con-A-coated Sepharose beads, but not lectin-free Sepharose beads, into the lumen of the left uterine horn of pseudopregnant mice on day 3 or 4 induced a decidual response that was virtually indistinguishable from that produced by blastocysts during normal pregnancy. The right uterine horn received no treatment and served as a control. Although the simultaneous administration of ⁴⁵CaCl₂ (1 mmol l^–1, 200 mCi mmol^–1) on day 3 of pseudopregnancy impeded this response, the deciduogenic potential of the Con-A-coated beads was not disrupted when these agents were simultaneously administered on day 4. This experiment with ⁴⁵CaCl₂ produced discrete areas of decidualization, as shown by the pontamine sky blue reaction on day 5 of pseudopregnancy. The decidualized areas contained significantly greater amounts of ⁴⁵Ca²⁺ than did the non-decidualized interjacent areas, indicating that the beads preferentially stimulated the rate of influx of the cation into these sites. Much of this cellular ⁴⁵Ca²⁺ content was lost in the early afternoon of day 5 of pseudopregnancy at a time when the luminal epithelium undergoes autolytic breakdown. The intraluminal introduction of 125 µg of Con A in solution (5 µl) was also deciduogenic but stimulated a larger uterine response than did the Con-A-coated beads and promoted a significantly greater uptake and retention of ⁴⁵Ca²⁺ than did the intraluminal injection of other agents. The results suggest that the embryonic signal responsible for induction of the decidual cell reaction in mice involves surface interactions between the embryo and uterine luminal epithelium to promote the influx of Ca²⁺ from the lumen into the epithelial cells and to modify their metabolism to stimulate the stromal cell transformations.

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