Fast action of estrogen on intracellular calcium in dormant mouse blastocyst and its possible mechanism.
OBJECTIVE
To study the fast action of estrogen on intracellular calcium of dormant mouse blastocysts and the possible mechanism.


METHODS
Controlled, prospective study.


METHODS
Academic research unit.


METHODS
Forty adult Kun-ming mice.


METHODS
A laser scanning confocal microscope was used to detect the dynamic change of intracellular calcium labeled by Fluo-3/AM, a fluorescent probe of calcium, which was caused by 17-beta-estradiol (17beta-E(2)) in dormant mouse blastocysts. A fluorescent microscope was used to check out the alteration of [Ca(2+)](i) induced by E(2)-BSA, a large molecule of estrogen coupling with bovine serum albumin; by 17beta-E(2) with Ca(2+)-free M2 medium; by 17beta-E(2) with tamoxifen, a blocking agent of traditional estrogen receptor (ER); and by 17beta-E(2) with U73122, a specific inhibitor of phospholipase C. Immunocytochemistry was used to detect the change of intracellular phosphorylated phospholipase C (p-PLC) induced by 17beta-E(2).


METHODS
Intracellular calcium and intracellular p-PLC in dormant mouse blastocysts.


RESULTS
Both 17beta-E(2) and E(2)-BSA could increase the intracellular calcium concentration ([Ca(2+)](i)) of blastocysts rapidly, and this increase of [Ca(2+)](i) was independent of either estrogen getting into the cells or the extracellular calcium in the incubation medium. However, this action was possibly blocked by a specific inhibitor of phospholipase C but not by the traditional blocking agent of ER. Moreover, the intracellular p-PLC increased after estrogen acting on blastocysts.


CONCLUSIONS
Estrogen may induce the increase of intracellular calcium in dormant mouse blastocysts by its action on the composition of the cell membrane to cause the release of Ca(2+) from the endoplasmic reticulum through the transmembrane signal transduction mediated by PLC.
Yu
Lin-lin
LL
Department of Physiology, West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, People's Republic of China.
Zhang
Jin-hu
JH
He
Ya-ping
YP
Huang
Ping
P
Yue
Li-min
LM
D000818:Animals; D001755:Blastocyst / Q000187:drug effects / Q000378:metabolism*; D020013:Calcium Signaling / Q000187:drug effects; D010064:Embryo Implantation; D004958:Estradiol / Q000378:metabolism*; D004963:Estrenes / Q000494:pharmacology; D004965:Estrogen Antagonists / Q000494:pharmacology; D005260:Female; D007150:Immunohistochemistry; D008297:Male; D051379:Mice; D018613:Microscopy, Confocal; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology; D010766:Phosphorylation; D011446:Prospective Studies; D011760:Pyrrolidinones / Q000494:pharmacology; D012710:Serum Albumin, Bovine / Q000378:metabolism*; D013629:Tamoxifen / Q000494:pharmacology; D013997:Time Factors; D010738:Type C Phospholipases / Q000037:antagonists & inhibitors / Q000378:metabolism
D004963:Estrenes; D004965:Estrogen Antagonists; D010726:Phosphodiesterase Inhibitors; D011760:Pyrrolidinones; C043090:estradiol-bovine serum albumin; D013629:Tamoxifen; C060229:1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione; D012710:Serum Albumin, Bovine; D004958:Estradiol; D010738:Type C Phospholipases