The re-epithelization of endometrium after menstrual desquamation

Ludwig, Hans; Metzger, Hildegard

doi:10.1007/bf00667681

Cited by 36 publications

(18 citation statements)

References 7 publications

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“…the in vivo responsiveness to 17␤-E2 is maintained in vitro. Oestrogens could not stimulate proliferation in endometria collected in the first 5 days of the menstrual cycle, when the surface epithelium that is damaged during menstruation is being repaired [24,25]. Only the basal layer, that contains the continuously dividing progenitor cells, is not (completely) shed during menstruation.…”

Section: Discussionmentioning

confidence: 90%

Triphasic pattern in the ex vivo response of human proliferative phase endometrium to oestrogens

Punyadeera¹,

Dunselman²,

Marbaix

et al. 2004

The Journal of Steroid Biochemistry and Molecular Biology

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Section: Discussionmentioning

confidence: 90%

Triphasic pattern in the ex vivo response of human proliferative phase endometrium to oestrogens

Punyadeera¹,

Dunselman²,

Marbaix

et al. 2004

The Journal of Steroid Biochemistry and Molecular Biology

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“…Diverse angiogenic stimuli arising from the perimenstrual endometrium are thought to control the initial phase of angiogenesis, which involves repair of the endometrial vasculature during the early follicular phase (50). However, this stimulation is unlikely to account for the persistence of angiogenesis in the luteal phase, which includes endothelial cell proliferating activity, increased microvascular density, and coiling of the spiral arteries (24,25,51).…”

Section: Discussionmentioning

confidence: 99%

Differential Effects of Thrombin and Hypoxia on Endometrial Stromal and Glandular Epithelial Cell Vascular Endothelial Growth Factor Expression

Lockwood¹,

Krikun²,

Koo³

et al. 2002

The Journal of Clinical Endocrinology & Metabolism

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Ovarian steroids and/or premenstrual endometrial hypoxia are thought to restore the endometrial vasculature shed during menstruation by elevating endometrial vascular endothelial growth factor (VEGF) levels. During the luteal phase, VEGF levels peak, progesterone induces estradiol (E(2))-primed human endometrial stromal cells (HESCs) to decidualize and express tissue factor (TF), and endometrial vascular permeability is enhanced. The latter would present circulating clotting factors to decidual cell-expressed TF to form local thrombin. HESCs were incubated in serum-supplemented medium containing vehicle (control) or 10(-8) M E(2) or 10(-7) M medroxyprogesterone acetate (MPA) or E(2) + MPA for 7 d to induce decidualization, while monolayers of human endometrial glandular epithelial cells (HEGECs) formed during 4-d incubation of glands. The medium was exchanged for a defined medium containing corresponding vehicle or steroids +/- thrombin under normoxia or hypoxia (0-1% O(2)). Hypoxia enhanced secreted immunoreactive VEGF levels by severalfold in HESCs and HEGECs, but the steroids did not affect VEGF output in either cell type under normoxia or hypoxia. In E(2) + MPA-decidualized HESCs, VEGF levels were elevated by 0.1 U/ml of thrombin, and 0.5-2.5 U/ml of thrombin elicited maximum effects. The addition of 0.5 U/ml of thrombin evoked a time-dependent enhancement of VEGF levels and about an 8-fold increase at 48 h (P < 0.02; n = 6). Northern blotting indicated that E(2) + MPA-decidualized HESCs expressed VEGF(121), VEGF(165), and VEGF(189) mRNA, which were enhanced severalfold during 5- to 20-h incubation with thrombin. Moreover, TRAP, a synthetic peptide activator of the constitutively expressed protease activated receptor-1 thrombin receptor in decidualized HESCs, also elevated secreted VEGF levels. By contrast, HEGECs were unresponsive to thrombin added alone or with ovarian steroids. These results suggest that thrombin formed by progestin-augmented TF levels acts as an autocrine enhancer of VEGF expression in decidualized HESCs. Because angiogenesis occurs in a matrix of decidualized HESCs, these in vitro results provide a novel mechanism to account for both the peak in VEGF and angiogenesis in luteal phase human endometrium.

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“…No stem cells were observed in the luminal surface (Spitzer et al 2012). Along this line, it was shown that re-epithelialization initiates around the remaining glandular stumps (Ludwig & Metzger 1976, Ludwig & Spornitz 1991. The contribution of the stem cells to endometrial regeneration following menses is still unclear.…”

Section: Inflammation-induced Regeneration Of Endometrial Tissuementioning

confidence: 99%

Endometrial inflammation and effect on implantation improvement and pregnancy outcome

2012

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Implantation failure, which is presently the major barrier in human fertility, is attributed, in many cases, to the failure of the uterus to acquire receptivity. The transition into a receptive uterus includes cellular changes in the endometrium and the modulated expression of different cytokines, growth factors, transcription factors, and prostaglandins. These molecules partake in the generation of an inflammatory response followed by the recruitment of immune cells. These cells have shown to be involved in the maternal immune tolerance toward the implanted embryo as well as in the maternal-fetus interaction during pregnancy. Most of the accumulated evidence indicates that embryo implantation is associated with an active Th1 inflammatory response while a Th2-humoral inflammation is required for pregnancy maintenance. Yet, recent findings suggest that a Th1 inflammatory response is also necessary for the acquisition of uterine receptivity. This notion was originally suggested by reports from our and other clinical centers worldwide that IVF patients with repeated implantation failure subjected to endometrial biopsy exhibit a substantial improvement in their chances to conceive. These findings, followed by the demonstration of an elevated pro-inflammatory cytokine/chemokine expression, as well as an increased abundance of immune cells, in the endometrium of these patients, raised the idea that acquisition of uterine receptivity is closely associated with an inflammatory response. This review summarizes the molecular and biochemical evidence that confirm this notion and proposes a mechanism by which injury-induced inflammation improves uterine receptivity and the subsequent pregnancy outcome.Reproduction (2012) 144 661-668

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The re-epithelization of endometrium after menstrual desquamation

Cited by 36 publications

References 7 publications

Triphasic pattern in the ex vivo response of human proliferative phase endometrium to oestrogens

Triphasic pattern in the ex vivo response of human proliferative phase endometrium to oestrogens

Differential Effects of Thrombin and Hypoxia on Endometrial Stromal and Glandular Epithelial Cell Vascular Endothelial Growth Factor Expression

Endometrial inflammation and effect on implantation improvement and pregnancy outcome

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