Garfield, R. E., Kannan, M. S., & Daniel, E. E. (1980). Gap junction formation in myometrium: control by estrogens, progesterone, and prostaglandins. The American Journal of Physiology, 238(3), C81-C89. https://doi.org/10.1152/ajpcell.1980.238.3.C81
Garfield RE, Kannan MS, Daniel EE. Gap junction formation in myometrium: control by estrogens, progesterone, and prostaglandins. Am J Physiol. 1980;238(3):C81-C89. doi:10.1152/ajpcell.1980.238.3.C81
Garfield, R. E., et al. "Gap junction formation in myometrium: control by estrogens, progesterone, and prostaglandins." The American Journal of Physiology, vol. 238, no. 3, 1980, pp. C81-C89.
Estrogen increased gap junctions in incubated immature rat myometrium
In a 1980 rat tissue study, estrogen increased the number of gap junctions in incubated uterine muscle from immature rats. Muscle fixed in place or soon after removal had none, and gap junctions formed once the tissue was incubated in a dish. Progesterone alone had no effect in the dish but lowered the number formed with estrogen.
Key Findings
In immature rats, estrogen injections with or without progesterone raised gap junction numbers after incubation, progesterone injections alone did not, and estrogen added in the dish also stimulated formation.
Progesterone added alone in the dish had no effect in any tissue, yet with estrogen it lowered gap junction numbers below estrogen alone in tissue from immature or pregnant rats.
No tissue fixed in place or shortly after removal showed gap junctions, which were present after 2 hours of incubation and grew in number and size up to 48 hours.
During incubation, tissue from immature rats formed far fewer gap junctions than tissue from pregnant or nonpregnant mature rats.
Indomethacin, 5,8,11,14-eicosatetraynoic acid and arachidonic acid partially inhibited gap-junction formation in incubated pregnant-rat tissue. A stable endoperoxide of prostaglandin H2 and arachidonic acid, unlike prostaglandins E1, E2 and F2α, overcame indomethacin's block.
Interpretation
This synopsis describes the published abstract only. The work is a laboratory study of uterine muscle, the myometrium, taken from pregnant, nonpregnant mature and immature rats. The researchers looked for gap junctions with two kinds of microscopy before and after the tissue was incubated in a dish. The researchers gave some immature rats hormone injections before removing their tissue and also treated tissue in the dish with hormones, prostaglandins and related compounds. The authors judge the results consistent with the idea that steroid hormones and prostaglandins interact to adjust how gap junctions form in uterine muscle.
RRM Context
RRM views estrogen and progesterone as partners whose balance matters, and cycle charting follows signs of each hormone across the cycle. Gap junctions join neighboring muscle cells so that signals can pass between them. The results suggest that this hormone balance may also act on the links between muscle cells in the rat uterus.
Our editorial summary of this paper, not the article's abstract.
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 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 with or without progesterone, but not with progesterone alone, increased the number of gap junctions found in tissues when incubated in vitro. In vitro treatment of tissues from immature animals with estrogen also stimulated the formation of gap junctions. Progesterone treatment in vitro had no effect on gap junction formation in any myometrial tissues. However, progesterone added in vitro in the presence of estrogen decreased the number of gap junctions as compared to the numbers formed with addition of estrogen alone in treated tissues from immature or pregnant animals. The addition of indomethacin 5,8,11,14-eicosatetraynoicacid and arachidonic acid partially inhibited the formation of gap junctions in tissues from pregnant animals incubated in vitro. A stable endoperoxide of PGH2 and arachidonic acid, but not PGE1, PGE2, PGF(2α), or thromboxane β2, overcame the inhibition of gap junction formation produced by indomethacin. These results are consistent with the hypothesis that steroid hormones and prostaglandin interact to modulate gap junction formation in the myometrium.
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