Gap junction formation in myometrium: control by estrogens, progesterone, and prostaglandins

Abstract

Myometrial tissues from pregnant and nonpregnant mature and immature rats were examined for the presence of gap junctions by thin section and freeze-fracture microscopy before and after incubation in vitro. Gap junctions were not present in any tissues fixed in situ or fixed shortly after removal from animals. The junctions were present in tissues incubated for 2 h in vitro, and the number and size of the junctions increased with increasing incubation times up to 48 h. Tissues from immature rats incubated in vitro formed gap junctions in much reduced numbers as compared to tissues from pregnant or nonpregnant mature animals. Injection of immature animals with estrogen [E] with or without progesterone [P], but not with P alone, increased the number of gap junctions found in tissues when incubated in vitro. In vitro treatment of tissues from immature animals with E also stimulated the formation of gap junctions. P treatment alone in vitro had no effect on gap junction formation in any myometrial tissues. P added in vitro in the presence of E decreased the number of gap junctions as compared to the numbers formed with addition of E alone in treated tissues from immature or pregnant animals. The addition of indomethacin, 5,8,11,14-eicosatetraynoic acid and arachidonic acid partially inhibited the formation of gap junctions in tissues from pregnant animals incubated in vitro. A stable endoperoxide of PG[prostaglandin]H2 and arachidonic acid, but not PGE1, PGE2, PGF2.alpha. or thromboxane B2, overcame the inhibition of gap junction formation produced by indomethacin. Steroid hormones and PG apparently interact to modulate gap junction formation in the myometrium.