Effect of estradiol-17ß and prostaglandins on rat myometrial gap junctions

MacKenzie, Leslie; Puri, Claudia; Garfield, R. E.

doi:10.1016/0090-6980(83)90155-7

Cited by 22 publications

(8 citation statements)

References 24 publications

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“…The amount of gap junctions in the myometrium increases at the time of labor, and their appearance are necessary for coordinating the contractile activity of the uterine smooth muscle required for the expulsion of the fetus (197, 198, 200,201,202,203, 440, 633). The expression of gap junctions in the uterine smooth muscle is controlled by endocrine factors with estrogens enhancing the expression and progesterone suppressing the expression of gap junctions (199, 232, 260, 406,407,408, 533, 563) (for more information see section on expression and trafficking). A very similar mechanism operates in the oviduct, where the number of gap junctions in the smooth muscle cells and the motor activity are increased by estrogens and decreased by progesterone (264,560).…”

Section: Physiological Function In Cell-to-cell Communicationmentioning

confidence: 99%

Gap Junctions

Nielsen,

Nygaard Axelsen,

Sorgen

et al. 2012

Comprehensive Physiology

381

365

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Gap junctions are essential to the function of multicellular animals, which require a high degree of coordination between cells. In vertebrates, gap junctions comprise connexins and currently 21 connexins are known in humans. The functions of gap junctions are highly diverse and include exchange of metabolites and electrical signals between cells, as well as functions, which are apparently unrelated to intercellular communication. Given the diversity of gap junction physiology, regulation of gap junction activity is complex. The structure of the various connexins is known to some extent; and structural rearrangements and intramolecular interactions are important for regulation of channel function. Intercellular coupling is further regulated by the number and activity of channels present in gap junctional plaques. The number of connexins in cell‐cell channels is regulated by controlling transcription, translation, trafficking, and degradation; and all of these processes are under strict control. Once in the membrane, channel activity is determined by the conductive properties of the connexin involved, which can be regulated by voltage and chemical gating, as well as a large number of posttranslational modifications. The aim of the present article is to review our current knowledge on the structure, regulation, function, and pharmacology of gap junctions. This will be supported by examples of how different connexins and their regulation act in concert to achieve appropriate physiological control, and how disturbances of connexin function can lead to disease. © 2012 American Physiological Society. Compr Physiol 2:1981‐2035, 2012.

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Section: Physiological Function In Cell-to-cell Communicationmentioning

confidence: 99%

Gap Junctions

Nielsen,

Nygaard Axelsen,

Sorgen

et al. 2012

Comprehensive Physiology

381

365

View full text Add to dashboard Cite

show abstract

“…High doses of estradiol stimulated my ornetrial gap junction development, whereas progesterone, when administered together with estradiol, suppressed myometuppo ported by Medical Research Council of Canada grants to Dr. W. E. Garfield. mature &s (Mac~enzie and Garfield 1985). Furthermore, inhibitors of cyclosxygenase administered to the nonpregnant animals together with estradiol enhanced the effect of the hormone on myometrial gap junctions (MacKenzie et al 1983;MacKenzie and Garfield 1985). Thus, these studies provided direct evidence and support the hypothesis that estrogen stimulates the presence of gap junctions in the myometrium.…”

Section: Introductionmentioning

confidence: 51%

Effects of 17β-estradiol on myometrial gap junctions and pregnancy in the rat

Mackenzie¹,

Garfield²

1986

Can. J. Physiol. Pharmacol.

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The effects of estradiol treatment on the development of myometrial gap junctions and premature labour were investigated using timed pregnant rats. In control animals myometrial gap junctions were infrequent between days 17 and 20 of pregnancy, but began to develop on day 21 and were at maximum frequency, size, and membrane area on day 22 during delivery. Gap junctions were completely absent from the myometrium 48 h after delivery. Animals treated with 500 micrograms 17 beta-estradiol/day starting on day 16 of pregnancy developed numerous myometrial gap junctions and delivered their pups prematurely on day 19. Similarly, treatment with 50 micrograms estradiol/day resulted in the development of myometrial gap junctions on day 20 of pregnancy and premature labour. However, treatment with various doses of estradiol up to and including 500 micrograms/day for 3 days beginning 1 day before delivery was not able to maintain the presence of myometrial gap junctions during the postpartum period. These results support the hypothesis that estradiol stimulates the development of myometrial gap junctions and that the presence of gap junctions in the myometrium is a requirement for the occurrence of term, as well as preterm labour. Furthermore, it is evident from this study that the postpartum regression of myometrial gap junctions is not dependent on the decrease in estradiol.

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“…It is evident, therefore, that estradiol stimulates the synthesis of gap junction proteins through the receptor mwhanisrn. It appears also that the prostaglandins we involved in the fomation of myornetrial gap junctions by regulating the effect of steroid hormones via decreasing the number or binding capacity of their receptors (Mackenzie et al 1983;MacKenzie and Garfield B 985).…”

Section: Note: Immature Rats Were Injected Daily For 4 Andmentioning

confidence: 97%

Effects of tamoxifen citrate and cycloheximide on estradiol induction of rat myometrial gap junctions

MacKenzie¹,

Garfield²

1986

Can. J. Physiol. Pharmacol.

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Longitudinal muscle of myometrial tissues from immature rats were examined by quantitative thin section electron microscopy for the presence of gap junctions after treatment with estradiol with and without tamoxifen, and cycloheximide for 1-6 days. Gap junctions were present between myometrial cells on days 4, 5, and 6 after treatment with estradiol (500 micrograms/day). Tamoxifen administered concomitantly with estradiol over the 6-day period completely prevented induction of the junctions. Gap junctions were not detected in the myometrium after treatment with tamoxifen alone. Administration of cycloheximide together with estradiol on day 0 of the 6-day period had no effect on gap junction frequency but resulted in a reduction in gap junction size in the myometrium after continued treatment with the hormone. Treatment with cycloheximide on day 1, however, significantly suppressed the effect of further estradiol treatment on the induction of gap junctions in the myometrium. Junctions were not visible in the tissues from animals treated with cycloheximide alone or in the control groups treated with sesame oil. These results indicate that estradiol influences the presence of gap junctions in the myometrium by regulating the synthesis of gap junction proteins through the steroid receptor mechanism.

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Effect of estradiol-17ß and prostaglandins on rat myometrial gap junctions

Cited by 22 publications

References 24 publications

Gap Junctions

Gap Junctions

Effects of 17β-estradiol on myometrial gap junctions and pregnancy in the rat

Effects of tamoxifen citrate and cycloheximide on estradiol induction of rat myometrial gap junctions

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