Telomerase expression in fertile patients compared to infertile patients with thin endometria

Lorch, Anja; Franco, Antonio Carlos Costa; McSweet, Juliette C.; Keefe, David L.; Kliman, Harvey J.

doi:10.1016/j.fertnstert.2004.07.189

Cited by 1 publication

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“…Decreased expression of telomerase in thin endometrium that is unresponsive to estrogen replacement therapy compared to normal endometrium indicates that thin endometrium may have a decrease of endometrial stem/progenitor cells [15]. Combined with the findings above, we hypothesize that chronic endometrial ischemia-associated stem/progenitor cell apoptosis may be involved in the pathogenesis of thin endometrium.…”

Section: Discussionmentioning

confidence: 76%

“…Changes in telomerase activity during the menstrual cycle reflect the proliferative potential of the endometrium [31]. Decreased expression of telomerase in thin endometrium that is unresponsive to estrogen replacement therapy compared with normal endometrium indicates that thin endometrium may have a decreased activity of endometrial stem/progenitor cells [15]. Pou5f1, as a nuclear transcription factor, encodes a transcription factor that is involved in mediating the maintenance of the undifferentiated state, and is widely regarded as a hallmark of pluripotent stem cells [29].…”

Section: Discussionmentioning

confidence: 99%

“…Endometrial stem/progenitor cells have critical roles in the physiological remodeling and regeneration of the human uterus and the pathogenesis of gynecological diseases, including endometriosis and endometrial cancer [13,14]. Lorch et al [15] determined that the average percentage of normal glands stained with telomerase was 94.5% on day 15 and 60% on day 24. With the diffuse pattern being present in 5.5% of nuclei on day 15 and no nuclei on day 24, the thin endometria had fewer mitotic figures on day 15, less telomerase staining on day 15(85%) and day 24(56%), and only 1.4% of the nuclei had diffuse staining on day 15 compared with normal endometria.…”

Section: Introductionmentioning

confidence: 99%

“…Telomerase is a reverse transcriptase whose activity is associated with the immortality of iPS cells (induced pluripotent stem cells), embryonic stem cells, germ cells and cancer cells [16–20]. Decreased expression of telomerase in thin endometrium, which is unresponsive to estrogen replacement therapy compared with that in normal endometrium, indicates that thin endometrium may have a decreased amount of endometrial stem/progenitor cells [15]. …”

Section: Introductionmentioning

confidence: 99%

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Decreased expression of c-kit and telomerase in a rat model of chronic endometrial ischemia

Yuan

2011

Med Sci Monit

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SummaryBackgroundIt was unclear whether chronic endometrial ischemia contributed to the pathogenesis of thin endometrium and was associated with decreased endometrial stem/progenitor cell. Thus, we explored the role of chronic endometrial ischemia in the pathogenesis of thin endometrium and its effect on endometrial stem/progenitor cells apoptosis.Material/MethodsIn vitro, endometrial side population (ESP) cell apoptosis models were built, and apoptosis was quantified by fluorescence-activated cell sorter (FACS) analysis, pou5f1, and c-kit mRNA was detected by qPCR. In vivo, a rat model of chronic endometrial ischemia was induced by performing bilateral uterine artery ligation. TERT and caspase3 were detected by immunohistochemistry. Pou5f1 and c-kit mRNA was examined by qPCR. C-kit, caspase3 and telomerase were detected by Western blot.ResultsIn the in vitro endometrial SP (ESP) cells apoptosis model, we found that the apoptotic rate was gradually increased with time, prolonging the expression of TERT, and c-kit mRNA was gradually decreased. In the in vivo endometrial SP (ESP) cells apoptosis model, we found that endometrial thickness, luminal epithelium thickness, gland epithelium thickness and the number of glands in the experiment group were significantly decreased compared with those in the control group (P<0.05). The expression levels of c-kit, pou5f1 and telomerase was significantly lower in the experimental group than those in the control group (P<0.05). The expression level of caspase3 was significantly higher in the experimental group compared with that in the control group (P<0.05).ConclusionsThe present work shows that chronic ischemia and chronic endometrial ischemia-associated stem/progenitor cells apoptosis may be responsible for the pathogenesis of thin endometrium.

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Section: Discussionmentioning

confidence: 76%