Estrogen and progesterone modulation of eosinophilic infiltration of the rat uterine cervix.
Ripening of the rat cervix involves widespread collagenolysis that follows an eosinophilic leukocyte infiltration. The hormonal control of these events is not well understood. The aims of this study were to investigate the mechanism through which progesterone (P) and 17beta-estradiol (E(2)) modulate eosinophilic invasion and to determine if this event is protein synthesis mediated. Cervical eosinophilic invasion was measured in intact rats during the second half of pregnancy and compared with values from ovariectomized (O) pseudopregnant (PSP) rats treated with P and E(2) in doses that mimicked the levels of pregnancy. Other O-PSP rats were treated with an E(2) antagonist (tamoxifen) and the antiprogestin RU-486. To study the role of protein synthesis in eosinophilic invasion of the cervix, rats were treated with actinomycin-D (an inhibitor of mRNA synthesis), and animals were sacrificed on D21 or D22 to evaluate eosinophilic invasion. Rats treated with E(2) showed high levels of infiltration and tamoxifen blocked this E(2) effect. On the other hand, P antagonized the stimulatory effects of E(2) on eosinophilic invasion, however when the P and E(2) treated rats were injected with RU-486 the inhibitory effect of P was reversed. In intact pregnant rats a sharp rise in eosinophilic infiltration was detected on D23, 20 h after the fall of serum P. Finally, E(2) treated rats injected with actinomycin-D had no invasion of eosinophils. In conclusion, the estrogen-triggered eosinophil invasion is affected by the classic estrogen receptor antagonist tamoxifen and by the mRNA synthesis blocker actinomycin-D suggesting a genomic action of E(2). Furthermore, the estrogen effect is blocked by P and this inhibition is reversed by RU-486.
Ramos
J G
JG
Department of Human Physiology, Faculty of Biochemistry and Biological Sciences, Universidad Nacional del Litoral, C. C. 530, Paraje El Pozo, Ciudad Universitaria, 3000, Santa Fe, Argentina.
Varayoud
J
J
Kass
L
L
Rodriguez
H
H
Muñoz de Toro
M
M
Montes
G S
GS
Luque
E H
EH
D000818:Animals; D020070:Cervical Ripening / Q000502:physiology; D002584:Cervix Uteri / Q000502:physiology*; D002634:Chemotaxis, Leukocyte / Q000187:drug effects / Q000502:physiology*; D003609:Dactinomycin / Q000494:pharmacology; D004804:Eosinophils / Q000502:physiology*; D004965:Estrogen Antagonists / Q000494:pharmacology; D004967:Estrogens / Q000494:pharmacology / Q000502:physiology*; D005260:Female; D015735:Mifepristone / Q000494:pharmacology; D019384:Nucleic Acid Synthesis Inhibitors / Q000494:pharmacology; D010052:Ovariectomy; D011247:Pregnancy; D011374:Progesterone / Q000494:pharmacology / Q000502:physiology*; D011555:Pseudopregnancy; D051381:Rats; D017208:Rats, Wistar; D013629:Tamoxifen / Q000494:pharmacology
D004965:Estrogen Antagonists; D004967:Estrogens; D019384:Nucleic Acid Synthesis Inhibitors; D013629:Tamoxifen; D003609:Dactinomycin; D015735:Mifepristone; D011374:Progesterone