Postpartum regeneration of the guinea pig endometrium: Relationship to serum estradiol and progesterone concentrations

Garris, David R.

doi:10.1002/ar.1092100107

Cited by 7 publications

(1 citation statement)

References 13 publications

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“…However, regeneration of uterine layers occurs following parturition in species with invasive placentation. This postpartum endometrial regeneration, or involution, is poorly understood in most species [32][33][34][35][36][37][38]. In mice, regeneration of the entire endometrium must occur at the sites of implantation.…”

Section: Introductionmentioning

confidence: 99%

Uterine Gland Formation in Mice Is a Continuous Process, Requiring the Ovary after Puberty, But Not after Parturition1

Stewart

Fisher

Wang

et al. 2011

Biology of Reproduction

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Uterine gland formation occurs postnatally in an ovary- and steroid-independent manner in many species, including humans. Uterine glands secrete substances that are essential for embryo survival. Disruption of gland development during the postnatal period prevents gland formation, resulting in infertility. Interestingly, stabilization of beta-catenin (CTNNB1) in the uterine stroma causes a delay in gland formation rather than a complete absence of uterine glands. Thus, to determine if a critical postnatal window for gland development exists in mice, we tested the effects of extending the endocrine environment of pregnancy on uterine gland formation by treating neonatal mice with estradiol, progesterone, or oil for 5 days. One uterine horn was removed before puberty, and the other was collected at maturity. Some mice were also ovariectomized before puberty. The hormone-treated mice exhibited a delay in uterine gland formation. Hormone-treatment increased the abundance of uterine CTNNB1 and estrogen receptor alpha (ESR1) before puberty, indicating possible mechanisms for delayed gland formation. Despite having fewer glands, progesterone-treated mice were fertile, suggesting that a threshold number of glands is required for pregnancy. Mice that were ovariectomized before puberty did not undergo further uterine growth or gland development. Finally, to establish the role of the ovary in postpartum uterine gland regeneration, mice were either ovariectomized or given a sham surgery after parturition, and uteri were evaluated 1 wk later. We found that the ovary is not required for uterine growth or gland development following parturition. Thus, uterine gland development occurs continuously in mice and requires the ovary after puberty, but not after parturition.

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Section: Introductionmentioning

confidence: 99%

Uterine Gland Formation in Mice Is a Continuous Process, Requiring the Ovary after Puberty, But Not after Parturition1

Stewart

Fisher

Wang

et al. 2011

Biology of Reproduction

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Scanning electron microscopic and morphometric analysis of the guinea pig uterine luminal surface: Cyclic and ovarian steroid-induced modifications

Garris

1998

Anat. Rec.

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A morphometric and scanning electron microscopic analysis of endometrial, luminal topographical changes of cyclic and ovariectomized, ovarian steroid-treated guinea pigs was undertaken to determine the effects of cyclic endocrine influences on the uterine surface features recognized to be involved in the process of interstitial blastocyst implantation. Estrogenic stimulation of the uterine epithelial layer induced microvillus growth and closed the endometrial gland openings on the luminal surface. Progestins antagonized these parameters, as indicated by short, sparse microvillus formation over a flat luminal uterine surface on which gland openings were both numerous and prominent. The combined effects of estrogen and progesterone therapies induced luminal epithelial changes resembling those characterizing the cyclic uterine surface at the time of blastocyst implantation. These data indicate that the cyclic alterations in the uterine luminal surface are directly regulated by ovarian steroid hormones, and that these changes in surface structure are synchronized and directly involved in the preparation for blastocyst-uterine interaction during the nidatory process in this species. Anat. Rec. 252:205-214, 1998. 1998 Key words: uterus; scanning electron microscopy; guinea pig; estrogens; progestins Scanning electron microscopy (SEM) has been used to study the luminal surface morphology of the oviduct (Dirksen and Satir 1972;Ferenczy et al., 1972;Kanagawa et al., 1972;Ludwig et al., 1972; Patek et al., 1972a,b;Dirksen, 1974;Rumery and Eddy, 1974), uterus (Psychoyos and Mandon,1971;Hafez, 1972Hafez, , 1973 Johnnisson and Nilsson, 1972;Anderson et al., 1975;Jones and Hamer, 1975;Ferenczy, 1974Ferenczy, ,1976Motta and Andrews, 1976;Garris, 1984d), and vagina (Kanagawa et al., 1972;Parakkal, 1974) in a number of species, including human (Ludwig et al., 1972, at various stages of the reproductive cycle. Cyclic changes in the rat uterine surface structure are recognized to be under ovarian steroid hormone control (Anderson et al., 1975). While estrogens potentiate microvillus formation by increasing both the number and length of each cell process, progesterone is recognized to induce a diminution in the density and length of uterine epithelial microvilli. As a result, the apical cell surface and intercellular borders of the epithelial cells are more pronounced under the influence of progestins than estrogens. However, the short cycle length and the lack of a functional corpus luteum following ovulation in the rat does not allow for the evaluation of the uterine luminal surface changes which occur as a result of estrogen and progesterone interaction during the prolonged luteal phase of the reproductive cycle.

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Effects of estradiol and progesterone on diabetes‐associated utero‐ovarian atrophy in C57BL/KsJ (db/db) mutant mice

Garris

1989

Anat. Rec.

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The modulating effects of estradiol (E: 1 microgram/3.5 days) and progesterone (P: 2 mg/3.5 days) on the obesity and hyperinsulinemic and hyperglycemic components of the diabetes-obesity syndrome in female C57BL/KsJ (db/db) mice, which includes cellular atrophy and adiposity in the reproductive tract, were examined and compared to corresponding control (+/?) parameters. All control and diabetic mice received oil (vehicle control), E, or P treatments starting at 4 weeks of age. Body weight, serum insulin levels, blood glucose concentrations, and utero-ovarian lipoprotein lipase activities were analyzed at 8 and 16 weeks of age and related to the ultrastructural changes in the steroid-sensitive uterine epithelium during the treatment period. Neither E nor P had any effect on body weights in (+/?) or (db/db) mice. The pronounced diabetes-associated elevation in serum insulin levels was enhanced by E, and suppressed by P, in 16-week-old (db/db) mice as compared with controls. By 16 weeks of age, the E therapy normalized blood glucose levels in diabetic mice to control levels, whereas P was ineffective in modulating the hyperglycemia. The reduction in blood glucose levels in E-treated diabetic mice correlated temporally with the return of normal intracellular structure including the disappearance of intracellular lipid vacuoles characteristic of uterine epithelium cells of (db/db) mice. The diabetes-induced rise in utero-ovarian lipoprotein lipase activity was normalized by P-therapy. The reduction in utero-ovarian lipoprotein lipase activity coincided temporally with the demonstrated intracellular reorganization in (db/db) reproductive tract tissues.(ABSTRACT TRUNCATED AT 250 WORDS)

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Postpartum regeneration of the guinea pig endometrium: Relationship to serum estradiol and progesterone concentrations

Cited by 7 publications

References 13 publications

Uterine Gland Formation in Mice Is a Continuous Process, Requiring the Ovary after Puberty, But Not after Parturition1

Uterine Gland Formation in Mice Is a Continuous Process, Requiring the Ovary after Puberty, But Not after Parturition1

Scanning electron microscopic and morphometric analysis of the guinea pig uterine luminal surface: Cyclic and ovarian steroid-induced modifications

Effects of estradiol and progesterone on diabetes‐associated utero‐ovarian atrophy in C57BL/KsJ (db/db) mutant mice

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