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Angiogenic factor imbalance precedes complement deposition in the placenta of preeclamptic-like BPH/5 mice

ABSTRACT: BPH/5 mice are an inbred strain with “borderline hypertension” that spontaneously develops both maternal and fetal hallmarks of preeclampsia. RNA-Seq analysis of BPH/5 uterine implantation sites at embryonic day 7.5, the peak of decidualization, identifies differential expression of inflammatory response genes, including members of the complement family, compared to C57 controls.

ORGANISM(S): Mus musculus

PROVIDER: GSE103670 | GEO | 2018/01/04

SECONDARY ACCESSION(S): PRJNA404000

REPOSITORIES: GEO

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Angiogenic factor imbalance precedes complement deposition in placentae of the BPH/5 model of preeclampsia.

Project description:Preeclampsia (PE), a hypertensive disorder of pregnancy, is a leading cause of maternal and fetal morbidity and mortality. Although the etiology is unknown, PE is thought to be caused by defective implantation and decidualization in pregnancy. Pregnant blood pressure high (BPH)/5 mice spontaneously develop placentopathies and maternal features of human PE. We hypothesized that BPH/5 implantation sites have transcriptomic alterations. Next-generation RNA sequencing of implantation sites at peak decidualization, embryonic day (E)7.5, revealed complement gene up-regulation in BPH/5 vs. controls. In BPH/5, expression of complement factor 3 was increased around the decidual vasculature of E7.5 implantation sites and in the trophoblast giant cell layer of E10.5 placentae. Altered expression of VEGF pathway genes in E5.5 BPH/5 implantation sites preceded complement dysregulation, which correlated with abnormal vasculature and increased placental growth factor mRNA and VEGF164 expression at E7.5. By E10.5, proangiogenic genes were down-regulated, whereas antiangiogenic sFlt-1 was up-regulated in BPH/5 placentae. We found that early local misexpression of VEGF genes and abnormal decidual vasculature preceded sFlt-1 overexpression and increased complement deposition in BPH/5 placentae. Our findings suggest that abnormal decidual angiogenesis precedes complement activation, which in turn contributes to the aberrant trophoblast invasion and poor placentation that underlie PE.-Sones, J. L., Merriam, A. A., Seffens, A., Brown-Grant, D.-A., Butler, S. D., Zhao, A. M., Xu, X., Shawber, C. J., Grenier, J. K., Douglas, N. C. Angiogenic factor imbalance precedes complement deposition in placentae of the BPH/5 model of preeclampsia.

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Transcriptome analysis of BPH-resistant and BPH-susceptible rice seedlings in response to BPH infestation

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Transcriptional alterations in BPH

Project description:We identified a BPH transcriptional signature that included 392 significantly differential expressed genes between BPH and control samples, and validated this BPH transcriptional signature using two independent study cohorts. By performing integrative analysis using transcriptional and methylation profiling, we identified two distinct BPH subtypes, supporting robust biologically distinct subgroups across different data types. To validate these BPH subtypes, we tested our signature via k-means clustering in two independent cohorts, and identified nearly identical subgroups. To nominate potential subtype specific therapeutic options, we utilized a Connectivity Map analysis, and found 50% of nominated compounds in one subgroup were related to inhibition of mTOR signaling.

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10x BPH sequencing on all cells

Project description:Single-cell mRNA sequencing (scRNA-seq) study was conducted to to probe heterogeneity of human BPH associated cells. No cell sorting was conducted so all cells within the BPH environment could be represented.

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Expression data from Incidental vs. Surgical BPH samples

Project description:used to identify differences between tissues from patients undergoing surgery for BPH with unresolved symptoms compared to incidental BPH from patients with prostate cancer

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Enhanced Reduced Representation Bisulfite Sequencing of BPH and control samples

Project description:We investigated the epigenetic landscape of benign prostatic hyperplasia (BPH) by defining the DNA methylation profile of 18 BPH samples and 5 controls from normal transitional zone. We identified 92,046 hypermethylated CpG and 10,117 hypomethylated CpG across different genomic regions in BPH, and hypermethylation was the dominant signal across all genomic regions, even when controlling for bias of CpG-rich loci. We defined a methylation signature for BPH that included 696 differentially methylated CpGs in promoter regions.

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