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• W2030264114 abstract "Biomarkers in MedicineVol. 3, No. 1 EditorialFree AccessNewly identified genes linked to endometrial receptiveness: lessons from IVFSamir Hamamah and Hervé DechaudSamir Hamamah† Author for correspondenceART/PGD Division, Arnaud de Villeneuve hospital, 34295-Montpellier, France. Search for more papers by this authorEmail the corresponding author at s-hamamah@chu-montpellier.fr and Hervé DechaudART/PGD Division, Arnaud de Villeneuve hospital, 34295-Montpellier, France. Search for more papers by this authorEmail the corresponding author at h-dechaud@chu-montpellier.frPublished Online:10 Feb 2009https://doi.org/10.2217/17520363.3.1.9AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareShare onFacebookTwitterLinkedInRedditEmail Figure 1. Ultrasonography is useful for evaluating endometrial receptivity.Figure 2. Endometrial profiles during the prereceptive and the receptive stages in natural and stimulated cycles.Hierarchical clustering between LH + 2 days and LH + 7 days samples, and between hCG + 2 days and hCG + 5 days samples. Red: upregulated genes; Green: downregulated genes.hCG: human chorionic gonadotropin; PR: Prereceptive; R: Receptive.A total of 30 years after the first in vitro fertilization (IVF) birth in the world, pregnancy and birth rates following IVF attempts remain low. Indeed, two out of three IVF cycles fail to result in pregnancy, and more than 9 out of 10 transferred embryos fail to implant [1]. Although the selection of high-quality embryos and endometrial status assessment have seen important technological progress, implantation rates are still low after controlled ovarian hyperstimulation (COS) for IVF [2]. Implantation failure is thought to result from impairment of embryo development and/or from abnormal uterine receptivity. The endometrium is receptive to blastocyst implantation during a spatially and temporally restricted window, ‘the implantation window’ [3]. In humans, this period begins 6–10 days after the lutenizing hormone (LH) surge and lasts approximately 48 h [4,5].Human endometrial receptivity during natural cyclesSuccessful implantation depends on synchronization between the developmental stages of the embryo itself and the complex series of molecular and cellular events induced in the endometrium by paracrine and autocrine regulators during the implantation window. This explains that there are many molecular marker candidates to determine the ‘ideal’ endometrium receptive period [6–10]. Several parameters have been suggested for assessing endometrial receptivity, including endometrial thickness (a classical criterion), endometrial morphology aspect and endometrial and subendometrial blood flow using ultrasonography and Doppler (Figure 1), noninvasive methods to evaluate uterine receptivity [6,7,9,11]. However, such indirect explorations result in controversy, and their positive predictive value is limited [12–14]. Emerging technology in the assessment of the gametes, competent embryos and endometrial receptivity, the omics allow the identification of biomarkers or to determine the molecular signature of endometrial cells specific to endometrial receptivity. More recently, transcriptomic approaches have been used to identify biomarkers of the human implantation window. Using microarray technology in human biopsy samples, several authors have observed modifications in gene expression profiles associated with the transition of the human endometrium from a prereceptive (LH + 2/4 days) to a receptive (LH + 7/9 days) state (Table 1)[15–19]. However, among the various regulated genes, only two genes were in common between all these studies: secreted phosphoprotein (SPP) 1, a glycoprotein involved in cellular adhesion and migration during embryo implantation, and IL15, a progesterone-regulated gene involved in stages immediately before, during and after the apposition step and permitting adequate proliferation of the stroma [20,21]. Disparities between these studies [15–19] may be explained by several factors: type of microarray used, data analysis, statistical methodologies, size of patient samples, ages of subjects and sampling time during the cycle. In addition, only two studies compared the early- and mid-secretory phases in the same patient [16,18], which seems a necessary condition to minimize the impact of interpatient variability. Incorporating these conditions and using a large series of patients (in contradiction to Riesewijk’s study), we identified four new biomarkers of endometrial receptivity that were upregulated in the LH + 7 days samples compared with the LH + 2 days samples. These biomarkers are MFAP5, ANGPTL1, EG-VEGF and NLF2, and play a role in the extracellular matrix remodeling of the endothelial cell microenvironment, angiogenesis and the formation of the endothelial fenestration. This group of genes shows potential to be useful prognostic markers of endometrium receptivity (Figure 2).Human endometrial receptivity during COS cyclesCOS is a key factor in the success of IVF–embryo transfer (ET). Studies comparing GnRH agonist long protocols with GnRH antagonist protocols remain controversial, and the impact of these protocols on endometrial receptivity has yielded conflicting results (Table 1)[22–26]. Several studies have shown that gene expression profiles associated with endometrial receptivity during COS (human chorionic gonadotropin [hCG] + 7/9) were closer to those in natural cycles (LH + 7/8), either under GnRH antagonist or agonist treatments [25,26]. However, the number of genes significantly modulated under COS in comparison with natural cycles was very different between these two studies (112 genes under GnRH antagonist treatment in Simon’s study vs 12 genes in Mirkin’s study; 122 genes under GnRH agonist treatment in the Simon’s study vs six genes in Mirkin’s study). Finally, Simon’s study concluded that endometrial development during cycles using GnRH antagonists was found to be histologically more similar to those from natural cycles than endometrium exposed to GnRH agonists [26]. Horcajadas’s study revealed that endometrial development was hampered during COS cycles, as judged by the number of genes significantly modulated under COS cycles in comparison with natural cycles (558 genes), showing gene expression levels more similar to those in a nonreceptive endometrium [24]. More precisely, they have demonstrated the existence of a 2-day delay in the activation/repression of two clusters composed of 218 and 133 genes, respectively, on day hCG + 7 versus LH + 7, affecting the endometrial receptivity process [22]. More recently, it has been reported that impairment of endometrial receptivity was due to a high concentration of steroids resulting from COS [23,27].Therefore, the real challenge is to perform COS treatment modifications to achieve a receptive endometrium that morphologically and functionally resembles the natural receptive endometrium, which will subsequently lead to improved success rates in IVF.Table 1. Number of genes significantly modulated in microarray comparison analyses between the early- and mid-secretory stages of the natural and stimulated endometrium cycle.StudyFirst sample: (number of samples)Second sample: (number of samples)Fold changeNumber of genesRef. UpDown Carson et al. (2002)LH + 2/4 (3)LH + 7/9 (3)≥2323370[15]Mirkin et al. (2005)LH + 3 (3)LH + 8 (5)≥24958[17]Riesewijk et al. (2003)LH + 2 (5)LH + 7 (5)≥315358[18]Talbi et al. (2006)ESP (3)MSP (8)≥1.514151463[19]Haouzi et al. (2009)LH + 2 (31)LH + 7 (31)≥294567[16]Mirkin et al. (2004)LH + 8 (5)LH + 8 (5)hCG + 9 Atg (5)hCG + 9 Ag (3)≥1.19≥1.26565[25]Horcajadas et al. (2005)LH + 7 (14)hCG + 7 (5)≥3281277[24]Simon et al. (2005)LH + 7 (14)LH + 7 (14)LH + 7 (14)hCG + 7 Atg standard dose (4)hCG + 7 Atg high dose (5)hCG + 7 Ag (5)≥22288226924100[26]Horcajadas et al. (2008)LH + 7 (5)LH + 9 (5)hCG + 7 (5)hCG + 9 (5)–690730[22]Liu et al. (2008)LH + 7 (5)LH + 7 (5)hCG + 7 high serum E2 levels (4)hCG + 7 low serum E2 levels (4)≥224451592[23]This table compares the number of genes significantly modulated between the LH + 2/4 and LH + 7/9 sample groups from five studies, as well as between LH + 7/9 days and hCG + 7/9 days sample groups from five other studies using the same approach.Ag: Agonist; Atg: Antagonist; ESP: Early-secretory phase; hCG: Human chorionic gonadotropin; LH: Leutenizing hormone; MSP: Mid-secretory phase.Financial & competing interests disclosureThe authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.No writing assistance was utilized in the production of this manuscript.Bibliography1 Kovalevsky G, Patrizio P: High rates of embryo wastage with use of assisted reproductive technology: a look at the trends between 1995 and 2001 in the United States. Fertil. Steril.84(2),325–330 (2005).Crossref, Medline, Google Scholar2 Donaghay M, Lessey BA: Uterine receptivity: alterations associated with benign gynecological disease. Semin. Reprod. Med.25(6),461–475 (2007).Crossref, Medline, CAS, Google Scholar3 Paria BC, Lim H, Das SK, Reese J, Dey SK: Molecular signaling in uterine receptivity for implantation. Semin. Cell Dev. Biol.11,67–76 (2000).Crossref, Medline, CAS, Google Scholar4 Martin J, Dominguez F, Avila S et al.: Human endometrial receptivity: gene regulation. J. Reprod. 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Metab.90(3) 1812–1818 (2005).Crossref, Medline, CAS, Google ScholarFiguresReferencesRelatedDetailsCited ByA Novel Molecule in Human Cyclic Endometrium: LncRNA TUNAR Is Involved in Embryo Implantation19 November 2020 | Frontiers in Physiology, Vol. 11 Vol. 3, No. 1 STAY CONNECTED Metrics History Published online 10 February 2009 Published in print February 2009 Information© Future Medicine LtdFinancial & competing interests disclosureThe authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.No writing assistance was utilized in the production of this manuscript.PDF download" @default.
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