Gene Expression Profiling of Neonatal Mouse Uterine Development1

Hu, Jianbo; Gray, Charles A.; Spencer, Thomas E.

doi:10.1095/biolreprod.103.026336

Cited by 51 publications

(72 citation statements)

References 29 publications

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“…By PND 12, endometrial glands extend from the LE into the surrounding endometrial stroma, and the outer longitudinal layer of the myometrium is fully organized into bundles [3]. The basic adult configuration of the uterus in mice is established by PND 15 [11]. Postnatal uterine morphogenesis is a critical period, because disruption of endometrial adenogenesis and mesenchymal specification and differentiation can cause permanent fertility problems in the adult [12][13][14].…”

Section: Introductionmentioning

confidence: 99%

Postnatal Deletion of Wnt7a Inhibits Uterine Gland Morphogenesis and Compromises Adult Fertility in Mice.

Dunlap¹,

Filant²,

Hayashi³

et al. 2011

Biology of Reproduction

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The success of postnatal uterine morphogenesis dictates, in part, the embryotrophic potential and functional capacity of the adult uterus. The definitive role of Wnt7a in postnatal uterine development and adult function requires a conditional knockout, because global deletion disrupts mü llerian duct patterning, specification, and cell fate in the fetus. The Wnt7a-null uterus appears to be posteriorized because of developmental defects in the embryo, as evidenced by the stratified luminal epithelium that is normally found in the vagina and the presence of short and uncoiled oviducts. To understand the biological role of WNT7A after birth and allow tissue-selective deletion of Wnt7a, we generated loxP-flanked exon 2 mice and conditionally deleted Wnt7a after birth in the uterus by crossing them with Pgr Cre mice. Morphological examination revealed no obvious differences in the vagina, cervix, oviduct, or ovary. The uteri of Wnt7a mutant mice contained no endometrial glands, whereas all other uterine cell types appeared to be normal. Postnatal differentiation of endometrial glands was observed in control mice, but not in mutant mice, between Postnatal Days 3 and 12. Expression of morphoregulatory genes, particularly Foxa2, Hoxa10, Hoxa11, Msx1, and Wnt16, was disrupted in the Wnt7a mutant uteri. Conditional Wnt7a mutant mice were not fertile. Although embryos were present in uteri of mutant mice on Day 3.5 of pregnancy, blastocyst implantation was not observed on Day 5.5. Furthermore, expression of several genes (Foxa2, Lif, Msx1, and Wnt16) was reduced or absent in adult Wnt7a-deleted uteri on Day 3.5 postmating. These results indicate that WNT7A plays a critical role in postnatal uterine gland morphogenesis and function, which are important for blastocyst implantation and fertility in the adult uterus.developmental biology, female reproductive tract, pregnancy, transgenic/knockout model, uterus

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Section: Introductionmentioning

confidence: 99%

Postnatal Deletion of Wnt7a Inhibits Uterine Gland Morphogenesis and Compromises Adult Fertility in Mice.

Dunlap¹,

Filant²,

Hayashi³

et al. 2011

Biology of Reproduction

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“…Therefore, it is important to understand the cellular and molecular mechanisms regulating postnatal development of the uterus. In mice, postnatal development of the endometrial glands and myometrium is initiated immediately after birth (Postnatal Day [PND] 0) and is completed by PND 15 [11,12].…”

Section: Introductionmentioning

confidence: 99%

Matrix Metalloproteinases and Their Tissue Inhibitors in the Developing Neonatal Mouse Uterus1

Hu¹,

Zhang²,

Nothnick³

et al. 2004

Biology of Reproduction

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Postnatal development of the mouse uterus involves differentiation and development of the endometrial glands as well as the myometrium. Matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) are involved in extracellular matrix breakdown and morphogenesis of many epitheliomesenchymal organs. As a first step to understanding their roles in postnatal mouse uterine development, MMPs and TIMPs found to be expressed in the neonatal mouse uterus by microarray analysis were localized by in situ hybridization. The MMP-2 mRNA was detected only in the uterine stroma, whereas the MMP-10 mRNA was present only in the uterine epithelium from Postnatal Day (PND) 3 to PND 9. All other MMPs (MMP-11, MMP-14, and MMP-23) as well as TIMP-1, TIMP-2, and TIMP-3 were detected in both epithelial and stromal cells of the endometrium, but not in the myometrium. Uterine extracts were then analyzed by gelatin and casein gel zymography to detect active gelatinases and stromelysins, respectively. Five major gelatinase bands of activity were detected and inhibited by the MMP inhibitors, EDTA or 1,10-phenanthroline, but not by PMSF, a serine protease inhibitor. Western blot analysis confirmed the presence of MMP-2 and MMP-9 proteins in the uterus. Immunoreactive MMP-9 protein was detected only in the endometrial stroma, whereas immunoreactive MMP-2 protein was detected in both the stroma and epithelium of the uterus. Casein zymography detected three major bands of activity ( approximately 54, 63, and 80 kDa) that were inhibited by the serine protease inhibitor, PMSF, but not by the MMP inhibitors, EDTA or 1,10-phenanthroline, suggesting that they were serine proteases. These results support the hypothesis that MMPs and TIMPs regulate postnatal development of the mouse uterus.

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“…Uterine gland development or adenogenesis is a postnatal event in rodents, domestic animals and humans (Hu et al 2004). At birth, murine uteri lack uterine glands and consist of simple luminal epithelium supported by undifferentiated mesenchyme.…”

Section: Endometrial Gland Developmentmentioning

confidence: 99%

Physiological and pathological implications of retinoid action in the endometrium

Jiang

Chen

Taylor

et al. 2018

Journal of Endocrinology

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Retinol (vitamin A) and its derivatives, collectively known as retinoids, are required for maintaining vision, immunity, barrier function, reproduction, embryogenesis and cell proliferation and differentiation. Despite the fact that most events in the endometrium are predominantly regulated by steroid hormones (estrogens and progesterone), accumulating evidence shows that retinoid signaling is also involved in the development and maintenance of the endometrium, stromal decidualization and blastocyst implantation. Moreover, aberrant retinoid metabolism seems to be a critical factor in the development of endometriosis, a common gynecological disease, which affects up to 10% of reproductive age women and is characterized by the ectopic localization of endometrial-like tissue in the pelvic cavity. This review summarizes recent advances in research on the mechanisms and molecular actions of retinoids in normal endometrial development and physiological function. The potential roles of abnormal retinoid signaling in endometriosis are also discussed. The objectives are to identify limitations in current knowledge regarding the molecular actions of retinoids in endometrial biology and to stimulate new investigations toward the development potential therapeutics to ameliorate or prevent endometriosis symptoms.

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Gene Expression Profiling of Neonatal Mouse Uterine Development1

Cited by 51 publications

References 29 publications

Postnatal Deletion of Wnt7a Inhibits Uterine Gland Morphogenesis and Compromises Adult Fertility in Mice.

Postnatal Deletion of Wnt7a Inhibits Uterine Gland Morphogenesis and Compromises Adult Fertility in Mice.

Matrix Metalloproteinases and Their Tissue Inhibitors in the Developing Neonatal Mouse Uterus1

Physiological and pathological implications of retinoid action in the endometrium

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