Project description:Whole-transcriptome profiles of individual human placental villi samples from twenty-five (25) Indian women with normal pregnancies during 6- to 8-weeks of gestation were examined using human whole genome expression arrays (NimbleGen 135K). The present study focused on the whole-transcriptome profiling using NimbleGen135K (070925_HG18_exp__12X135K) human whole genome expression arrays of individual human placental villi samples obtained from twenty-five (25) proven-fertile women bearing normal pregnancies voluntarily terminated between 6- and 8-weeks of gestation. Gestational age was estimated from menstrual history, physical and ultrasonographic evaluation. No case of complicated pregnancy from infection, and other significant fetal and maternal clinical indications was included. These twenty five (25) samples include biological replicates of 6, 7 and 8 weeks placental villi samples.
Project description:Whole-transcriptome profiles of individual human placental villi samples from twenty-five (25) Indian women with normal pregnancies during 6- to 8-weeks of gestation were examined using human whole genome expression arrays (NimbleGen 135K).
Project description:Identification of factors in conditioned media of first-trimester placental villous explants. Explants were cultured under hypoxia (2% O2), 5% CO2 in serum-free DMEM/F12 and treated with recombinant galectin-7 (1ug/ml) or vehicle control (BSA) for 72h. Identification of factors in conditioned media of first-trimester placental villous explants. Explants were cultured under superoxia (20% O2), 5% CO2 in serum-free DMEM/F12 and treated with recombinant galectin-7 (1ug/ml) or vehicle control (BSA) for 72h.
Project description:To explore the influence of maternal choline intake on placental gene expression, we employed whole genome microarray expression profiling to identify genes that were differentially expressed in placental tissues obtained from women consuming two different doses (480 vs. 930 mg/d) of choline throughout the third trimester of pregnancy. Healthy third trimester (gestational week 26-29) pregnant women were randomized to a 12-week choline controlled feeding study. The participants consumed either 480 (n=6) or 930 (n=6) mg choline/d. Full thickness placental samples were collected at delivery to extract RNA and perform the arrays. Healthy third trimester (gestational week 26-29) pregnant women were randomized to a 12-week choline controlled feeding study. The participants consumed either 480 (n=6) or 930 (n=6) mg choline/d for 12 weeks. Placental samples were obtained at delivery
Project description:To explore the influence of maternal choline intake on placental gene expression, we employed whole genome microarray expression profiling to identify genes that were differentially expressed in placental tissues obtained from women consuming two different doses (480 vs. 930 mg/d) of choline throughout the third trimester of pregnancy. Healthy third trimester (gestational week 26-29) pregnant women were randomized to a 12-week choline controlled feeding study. The participants consumed either 480 (n=6) or 930 (n=6) mg choline/d. Full thickness placental samples were collected at delivery to extract RNA and perform the arrays.
Project description:The human intraplacental environment undergoes major changes at the end of the first trimester associated with onset of the maternal blood flow. We collected placental villi samples before and after maternal blood flow to profile methylation changes at this crucial time window.
Project description:Miscarriage occurs in 15-20% of clinical pregnancies. While chromosomal errors are observed in over 50%, causes of karyotypically normal losses are poorly understood. DNA methylation undergoes reprogramming during development and must be appropriately set to maintain a healthy pregnancy. We hypothesize that aberrant DNA methylation may cause karyotypically normal miscarriage, particularly among women experiencing recurrent miscarriage (RM). DNA methylation in first trimester chorionic villi was assessed in chromosomally normal miscarriages from women with RM (N=33) or isolated miscarriage (M, N=21), and elective terminations (TA, N=16). Differentially methylated candidate loci were identified using the Illumina Infinium HumanMethylation27 BeadChip array by comparing 10 RM to 10 TA samples. Follow up showed a significant increase in methylation in RM and M compared to TA placentae at the CYP1A2 (p=0.002) and AXL (p=0.02) promoters and decrease at the DEFB1 (p=0.008) promoter. Gene function analysis showed an enrichment of imprinted genes (p=9.53E-10) and genes previously associated with RM (p=9.51E-06). DNA methylation was evaluated at 7 imprinted loci using bisulfite pyrosequencing. An increase of outliers at these loci was observed in RM (3.9%) compared to M (0%) and TA (0.9%) (p=0.02), with increased average methylation at the H19/IGF2 ICR1 in M samples (p<0.0001). Altered DNA methylation in the placenta at specific loci, as well as global dysregulation in specific cases, may contribute to or be a consequence of placental insufficiency in karyotypically normal miscarriage. First-trimester placental villi samples from karyotypically normal miscarriages from recurrent miscarriage patients (N, N=10) and chromosomally normal elective terminations (PZET, N=10).
Project description:To identify the proteins and molecular signaling pathways that contribute to EPL, we performed proteomics and bioinformatics analysis of the placental villi in women who have undergone EPL and in normal pregnant women.
Project description:To identify the proteins and molecular signaling pathways that contribute to EPL, we performed proteomics and bioinformatics analysis of the placental villi in women who have undergone EPL and in normal pregnant women.