Comparison of endometrial expression in patients which underwent previous recurrent abortions, implantation failure after IVF/ICSI compared to control fertile
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Nathalie Lédée
PROVIDER: E-GEOD-26787 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Molecular mechanisms responsible for abnormal endometrial vasculature in women receiving long-acting progestin-only contraceptives (LAPCs) are unknown. We hypothesize that LAPCs impairs vascular smooth muscle cell (VSMC) and pericyte proliferation and/or migration producing thin-walled hyperdilated fragile microvessels prone to bleeding. Proliferating cell nuclear antigen (PCNA) and alpha smooth muscle actin (aSMA) double-immunohistochemistry assessed VSMC differentiation and proliferation in endometria from women pre- and postDepoProvera (Depo) treatment and from oophorectomized guinea pigs (OVX-GPs) treated with vehicle, estradiol (E2), medroxyprogesterone acetate (MPA) or E2+MPA pellets. After treating cultured VSMCs with MPA or etonogestrel (ETO), whole genome profiling, proliferation and migration assays were performed. Endometrial vasculature of Depo-administered women displayed reduced M-DM-.SMA immunoreactivity and fewer PCNA (+) nuclei among aSMA (+) cells (P<0.008). Microarray analysis of VSMCs identified several MPA and ETO-altered transcripts regulated by STAT1 signaling (p<2.22x10-6), including chemokine (C-C motif) ligand 2 (CCL2). Both MPA and ETO reduced VSMC proliferation and migration (p<0.001), recombinant CCL2 reversed this progestin inhibition, and, in turn, a STAT1 inhibitor abolished these CCL2 effects. Similarly, the endometria of MPA treated OVX-GPs displayed decreased aSMA staining and fewer PCNA (+) nuclei in VSMC (p<0.005). In conclusion, LAPCs promote abnormal endometrial vessel formation by inhibiting VSMC proliferation and migration. Total RNA (n=3) obtained from cultured TDCs incubated 6h with estradiol or estradio + medroxyprogesterone acetate with or without 1 ng/ml IL-1M-NM-2 for 6h.
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Project description:BackgroundCalcium (Ca2+) ionophores are now mainly considered as efficient treatments for fertilization failure. Recently, its application for rescuing poor embryo development was proposed but still non-routine. This study aimed to explore whether Ca2+ ionophore improves embryo development and pregnancy outcomes in patients with poor embryo development in previous intracytoplasmic sperm injection (ICSI) cycles.MethodsThis study included 97 patients undergoing assisted oocyte activation (AOA) with Ca2+ ionophore (calcimycin, A23187) treatment. Preimplantation embryonic development and clinical outcomes were compared between ICSI-AOA cycles (AOA group) and previous ICSI cycles of the same patients in which poor embryo developmental potential was present (non-AOA group). Subgroups stratified by maternal age (< 35, 35-40, ≥ 40 years, respectively) were analyzed separately.ResultsA total of 642 MII oocytes were collected in AOA group, and 689 in non-AOA group. Significantly higher day 3 good quality embryo rate (P = 0.034), good quality blastocyst formation rate (P < 0.001), and utilization rate (P < 0.001) were seen in AOA group. Similar results were seen in each subgroup. For pregnancy outcomes, there were significant differences in clinical pregnancy rate (P = 0.039) and live birth rate (P = 0.045) in total group. In subgroup aged < 35 years, biochemical (P = 0.038), clinical (P = 0.041), and ongoing pregnancy rate (P = 0.037) in AOA group were significantly higher than that in non-AOA group. No significant improvement for clinical outcomes for subgroups aged 35-40 and aged ≥40.ConclusionThe study suggests that calcimycin could improve preimplantation development and pregnancy outcomes in patients aged < 35 years with embryo developmental problems in previous ICSI cycles.
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