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Placental Growth Factor/Nrp-1 signaling is required for medulloblstoma growth

ABSTRACT: Here we present that growth of medulloblastoma is dependent on PlGF/Nrp-1 signaling. PlGF and Nrp-1 are expressed across different molecular subgroups of medulloblastoma. Data presented here are part of a combined molecular effort to subclassify our medulloblastoma cohort according to current molecular criteria (Taylor et al., 2011). Furthermore, we include aCGH of two medulloblastoma cell lines that were used as models in our experiments.

ORGANISM(S): Homo sapiens

PROVIDER: GSE37412 | GEO | 2012/10/01

SECONDARY ACCESSION(S): PRJNA159941

REPOSITORIES: GEO

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Placental Growth Factor/Nrp-1 signaling is required for medulloblstoma growth

Project description:Here we present that growth of medulloblastoma is dependent on PlGF/Nrp-1 signaling. PlGF and Nrp-1 are expressed across different molecular subgroups of medulloblastoma. Data presented here are part of a combined molecular effort to subclassify our medulloblastoma cohort according to current molecular criteria (Taylor et al., 2011). Furthermore, we include aCGH of two medulloblastoma cell lines that were used as models in our experiments. Analyses were performed on 32 archival specimens of medulloblastoma, WHO Grade IV, seen at the Department of Pathology, Massachusetts General Hospital from 1998 to 2009. aCGH data included are for two medulloblastoma cell lines, D283 and D341, and 6 clinical cases for which DNA (good quantity and quality) was available.

2012-10-01 | E-GEOD-37412 | biostudies-arrayexpress

Arabidopsis NRP switches off the PP6 phosphatase FyPP3 to repress auxin-mediated growth in response to abscisic acid

Project description:How environmentally challenged plants can switch from growth to stress adaptation is an important question in plant physiology. To identify the key regulatory proteins and to characterize the underlying signaling pathways are essential in answering this question. Here we show that the abiotic stress hormone Abscisic acid (ABA) induces the expression of the Asparagine rich proteins (NRP), DCD1 and DCD2, to repress the auxin-induced growth by promoting vacuolar degradation of PIN2, the auxin efflux carrier. ABA-induced degradation of PIN2 is inhibited in the dcd1 dcd2 double mutant, and inhibition of FyPP3, the catalytic subunit of the PP6 protein phosphatase, can restore the PIN recycling and growth phenotype in the double mutant. Transcriptome analyses on WT, dcd1 dcd2, the FyPP3 Dominant Negative line (FyPP3-DN), and dcd1 dcd2/FyPP3-DN supported the essential function of the NRP-FyPP3 module in the growth- to stress-response switch.

2020-05-16 | GSE150648 | GEO

NRP histone chaperones promote the removal of histone variant H2A.Z

Project description:In eukaryotes, DNA wraps around histones to form nucleosomes, which are compacted into chromatin. DNA-templated processes, including transcription, require chromatin disassembly and reassembly mediated by histone chaperones. Additionally, distinct histone variants can replace core histones to regulate chromatin structure and function. Although replacement of H2A with the evolutionarily conserved H2A.Z via the SWR1 histone chaperone complex has been extensively studied, in plants little is known about how a reduction of H2A.Z levels can be achieved in plants. Here, we show that NRP proteins cause a decrease of H2A.Z-containing nucleosomes in Arabidopsis under standard growing conditions. nrp1-1 nrp2-2 double mutants show an over-accumulation of H2A.Z genome-wide, especially at heterochromatic regions normally H2A.Z-depleted in wild-type plants. Our work suggests that NRP proteins regulate gene expression by counteracting SWR1, thereby preventing excessive accumulation of H2A.Z.

2020-04-29 | GSE127986 | GEO

Placental Growth Factor Regulates the Pentose Phosphate Pathway and Antioxidant Defense Systems in Human Retinal Endothelial Cells

Project description:The molecular mechanisms whereby placental growth factor (PlGF) mediates its effects in nonproliferative diabetic retinopathy (DR) are unknown. To better understand the role of PlGF in DR, we used tandem mass tags (TMT)-labeled quantitative proteomics to human retinal endothelial cells (HRECs), treated anti-PlGF antibody as a experimental, PBS as a control.

2020-03-17 | PXD017195 | Pride

Comparison of gene expression by microarray in diabetes antigen specific (NRP-V7), LCMV antigen specific (GP33), and CD8+ T cells of similar phenotype from NOD mice

Project description:Type 1 diabetes mellitus (T1D) is caused by killing of insulin producing β cells by CD8+T cells. The disease progression accelerates as glucose tolerance deteriorates suggesting that acquired factors contribute. To identify how environmental factors may lead to the expansion and pathogenicity of the diabetogenic T cells, we analyzed diabetogenic NRP-V7-reactive CD8+ T cells that recognize a peptide from the diabetes antigen IGRP in prediabetic NOD mice. There was an increase in the frequency of the NRP-V7-reactive cells coinciding with the time of glucose intolerance. The T cells persisted in hyperglycemic NOD mice maintained with an insulin pellet despite destruction of beta cells. We compared gene expression in the NRP-V7-reactive T cells to others that shared their phenotype but not selected for reactivity to diabetes antigens viral antigen reactive cells. Compared to these other cells, the NRP-V7-reactive cells exhibited gene expression of memory precursor effector cells. They had reduced cellular proliferation and were less dependent on oxidative phosphorylation. When prediabetic NOD mice were treated with 2DG to block aerobic glycolysis, there was a reduction in the diabetes antigen vs other cells of similar phenotype and loss of lymphoid cells infiltrating the islets. In addition, treatment of NOD mice with 2DG resulted in improved cell granularity. These findings identify a link between metabolic disturbances and autoreactive T cells that promotes development of autoimmune diabetes.

2016-03-17 | GSE79200 | GEO

Placental growth factor as potential target against hepatocellular carcinoma in an orthotopic mouse model.

Project description:The placental growth factor (PlGF) is member of the vascular endothelial growth factor (VEGF)-family known to stimulate endothelial cell growth, migration and survival, attract angiocompetent macrophages and bone marrow progenitor cells and determine the metastatic niche. Unlike VEGF, genetic studies have shown that PlGF is specifically involved in the pathologic angiogenesis, thus its inhibition would not affect healthy blood vessels, providing an attractive drug candidate with a good safety profile. In this study, we assess whether inhibition of PlGF could be used as a potential therapy against hepatocellular carcinoma (HCC), by using PlGF-knock out mice and monoclonal antibodies targeting PlGF in an orthotopic model for HCC. In addition, the effect of PlGF-antibodies is compared to that of Sorafenib, as well as the combination of both therapies. In our study we have found that both in a transgenic knock out model as in a treatment model, silencing or inhibition of PlGF significantly decreased tumour burden, not only by inhibiting the vascularisation, but also by decreasing hepatic macrophage recruitment and by normalizing the remaining blood vessels, thereby decreasing hypoxia and thus, reducing the pro-metastatic potential of HCC. Conclusion: considering its favourable safety profile and its pleiotropic effect on vascularisation, metastasis and inflammation, targeting PlGF could become a valuable therapeutic strategy against HCC.

2014-12-23 | GSE35289 | GEO

NRP histone chaperones promote the removal of histone variant H2A.Z

Project description:NRP histone chaperones promote the removal of histone variant H2A.Z

| PRJNA525997 | ENA

Gene expression changes induced in mouse bone marrow by placenta growth factor (PlGF) overexpression.

Project description:Placenta growth factor (PlGF) is a member of the vascular endothelial growth factor family and plays an important role in adult pathological angiogenesis. To further investigate PlGF functions in tumor growth and metastasis formation, we used transgenic mice overexpressing PlGF. Recent studies demonstrate that tumor vascularization does not exclusively rely on preexisting vessels but also depends on bone marrow derived progenitor cells. The aim of the present work is to investigate the effect of the PlGF overexpression in the skin on the transcriptional landscape of bone marrow derived cells.

2021-11-01 | GSE52414 | GEO

Placental growth factor mediates pathological uterine vasculature by activating the NFAT5-SGK1 mechano-signaling axis in the endometrium: Implications for pre-eclampsia development.

Project description:After menstruation the uterine spiral arteries are repaired through angiogenesis. This process is tightly regulated by the paracrine communication between endometrial stromal cells (EnSCs) and endothelial cells. Any molecular aberration in these processes can lead to complications in pregnancy including miscarriage or pre-eclampsia (PE). Placental growth factor (PlGF) can increase cell stiffness contributing to pathological angiogenesis but the biomechanisms remain poorly understood. In this study, we investigated whether PlGF contributes to pathological uterine vasculature by disrupting EnSCs and endothelial paracrine communication. We observed that PlGF mediates a tonicity-independent activation of nuclear factor of activated T cells 5 (NFAT5) in EnSCs. NFAT5 activated downstream targets including SGK1, HIF-1α and VEGF-A. In depth characterization of PlGF - conditioned medium (CM) from EnSCs using mass spectrometry and ELISA methods revealed low VEGF-A and an abundance of extracellular matrix organization associated proteins. Secreted factors in PlGF-CM impeded normal angiogenic cues in endothelial cells (HUVECs) by downregulating Notch-VEGF signalling. Interestingly, PlGF-CM failed to support human placental (BeWo) cell invasion through HUVEC monolayer. Inhibition of SGK1 in EnSCs improved angiogenic effects in HUVECs and promoted BeWo invasion, revealing SGK1 as a key intermediate player modulating PlGF mediated anti-angiogenic signalling. Taken together, perturbed PlGF-NFAT5-SGK1 mechano-signaling in the endometrium can contribute to pathological uterine angiogenesis by negatively regulating EnSCs -endothelial crosstalk resulting in poor quality vessels in the uterine microenvironment. Taken together the signaling may impact on normal trophoblast invasion and thus placentation and, may be associated with an increased risk of complications such as PE.

2024-10-17 | PXD051697 | Pride

Deep Sequencing Identifies IDH1 R132S Mutation in Adult Medulloblastoma (CGH)

Project description:Here we present the case of adult medulloblastoma with minimal chromosomal rearrangements. Data presented here are aCGH analyses of two biopsies of adult patient with a medulloblastoma which was classified as a Shh subgroup.

2013-01-01 | GSE41990 | GEO

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