Radioligand and immunochemical studies of turtle oviduct progesterone and estrogen receptors: correlations with hormone treatment and oviduct contractility.
Progesterone (PR) and estrogen (ER) receptors were previously identified and characterized in the reproductive tract of the turtle, Chrysemys picta, and changes in PR levels were monitored during the seasonal cycle. To understand the hormonal regulation of PR, intact and ovariectomized animals were treated with estradiol, progesterone, and a combination of estradiol and progesterone, and high affinity PR and ER levels were determined by radioligand binding studies. Ovariectomy significantly decreased ER levels; in contrast, PR levels increased following ovariectomy. In both intact and ovariectomized animals, estradiol alone did not elevate PR levels above control; however, the PR was down-regulated by progesterone. ER levels in ovariectomized animals were not restored by any of the steroid regimens. By Western blot analysis, PR levels appeared to increase following ovariectomy, were unaffected by estradiol, and were somewhat decreased following progesterone treatment in estradiol-primed ovariectomized animals. While not quantitative, these results are supportive of radioligand binding studies. Immunocytochemical studies of oviduct PR followed the same pattern showing increased immunoreactivity following ovariectomy, no change with estradiol, and a decrease following progesterone treatment of estradiol-primed animals. Oviduct contractility was monitored as a physiological index of progesterone action. Estradiol significantly increased the amplitude of the contractions both in vivo and in vitro, whereas progesterone in combination with estradiol significantly inhibited the estrogen effect. This study suggests that estradiol alone may not be adequate for regulation of both ER and PR. While progesterone down-regulates its own receptor, it does not appear to influence the ER. These data are in contrast to mammalian and avian studies which show that estradiol increases both the ER and PR in the reproductive tract, and progesterone down-regulates both receptors.
Giannoukos
G
G
Department of Biology, Boston University, Massachusetts 02215, USA.
Callard
I P
IP
D000645:Ammonium Sulfate; D000818:Animals; D015153:Blotting, Western; D002467:Cell Nucleus / Q000378:metabolism; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D007700:Kinetics; D009119:Muscle Contraction / Q000187:drug effects; D009215:Myometrium / Q000187:drug effects / Q000378:metabolism; D010052:Ovariectomy; D010057:Oviducts / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D011374:Progesterone / Q000494:pharmacology*; D011869:Radioligand Assay; D011960:Receptors, Estrogen / Q000187:drug effects / Q000378:metabolism*; D011980:Receptors, Progesterone / Q000187:drug effects / Q000378:metabolism*; D014426:Turtles / Q000378:metabolism*
D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D011374:Progesterone; D004958:Estradiol; D000645:Ammonium Sulfate