Expression profiling of microglia lacking Tgfbr2
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ABSTRACT:
PROVIDER: PRJNA514041 | ENA |
REPOSITORIES: ENA
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Project description:Microglia contribute to maintaining brain homeostasis by interacting with neurons and macroglial cells through different signaling molecules. Here, we investigate the transcriptional profile of microglia lacking TGFbeta signaling given by inactivation of the Tgfbr2 gene, at three different stages of development. These microglia show a signature consistent with increased activation and impaired maturation, representing a state commonly associated with neurological pathologies.
2019-01-10 | GSE124868 | GEO
Project description:Transcriptional profiling of endothelial cells lacking Tgfbr2
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Project description:Tgfbr2 controls signal transduction after binding activated Tgfb1. Inactivation of this receptor in endothelium results in vascular dysplasia and severe hemorrhage. Here, we define the transcriptional profile of endothelial cells lacking Tgfbr2.
2020-05-06 | GSE146487 | GEO
Project description:Transcriptomes of Tgfbr2 Knockout Microglia and Macrophages
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Project description:The cytokine transforming growth factor-B (TGF-B) regulates development and homeostasis of several tissue-resident macrophage populations, including microglia. TGF-B is not critical for microglia survival, but is required for the maintenance of the microglia-specific homeostatic gene signature. Under defined host conditions circulating monocytes can compete for the microglial niche and give rise to long-lived monocyte-derived macrophages residing in the central nervous system (CNS). Whether monocytes require TGF-B for colonization of the microglial niche and maintenance of CNS integrity is unknown. We found that abrogation of TGF-B signaling in CX3CR1+ monocyte-derived macrophages led to rapid onset of a progressive and fatal demyelinating motor disease characterized by myelin-laden giant macrophages throughout the spinal cord. The devastating motor disease that developed in TGF-BR2-deficient chimeras indicated that in the absence of TGF-B signaling the CNS environment licenses monocyte-derived macrophages for tissue damage. We therefore addressed how the gene expression signature of CNS macrophages was controlled by TGF-B signaling. We thus sorted TGF-BR2-deficient monocyte-derived macrophages from animals with ongoing motor disease and from their wildtype littermate counterparts. For comparison we sorted wild-type and TGF-BR2-deficient microglia and performed RNA sequencing for all four groups. Tgfbr2-deficient macrophages were characterized by high expression of genes encoding proteins involved in antigen presentation, inflammation and phagocytosis. TGF-B is thus crucial for the functional integration of monocytes into the CNS microenvironment.
2018-04-16 | GSE111385 | GEO
Project description:Transforming growth factor beta receptor 2 (Tgfbr2) was predicted as a causal gene for abdominal using a novel statistical method named LCMS (Schadt et al., 2005, Nature Genetics). In order to validate this prediction, we profiled the liver tissues of Tgfbr2 heterozygous knockout mice (Tgfbr2+/-) and their littermate wild-type (wt) controls to examine the gene expression signature as well as pathways/networks resulting from the single gene perturbation. 6 Tgfbr2+/- mice and 4 wt controls were profiled. Reference pool included RNA extracted from the liver of 6 wt control mice. Dye-swap was involved in the profiling.
2009-03-07 | E-GEOD-11994 | biostudies-arrayexpress
Project description:Microsatellite unstable (MSI) colorectal cancers (CRCs) are characterized by Transforming Growth Factor Beta Receptor Type 2 (TGFBR2) deficiency. TGFBR2-deficient CRCs present altered target gene and protein expression. Such cellular alterations modulate the content of CRC-derived extracellular vesicles (EVs). EVs function as couriers of proteins, nucleic acids, and lipids in intercellular communication. At a qualitative level, we have previously shown that TGFBR2 deficiency can cause overall alterations in the EV protein content. To deepen the basic understanding of altered protein dynamics, this work aimed to quantify EV protein signatures in a TGFBR2-dependent manner. Using a SILAC approach for mass spectrometry-based quantification, 48 proteins that appeared to be regulated by cellular TGFBR2 expression were identified in MSI-derived EVs. TGFBR2-primed EVs were enriched in proteasome-associated proteins, whereas TGFBR2 deficiency led to upregulation of EV proteins related to the extracellular matrix and nucleosome. Altogether, the present study emphasizes the general overlap of proteins between EVs and their parental CRC cells and highlights the pathological role of the MSI tumor driver mutation affecting TGFBR2 by altering protein landscapes of EVs. From a clinical perspective, TGFBR2-regulated quantitative differences of protein expression in EVs might nominate novel biomarkers for liquid biopsy-based MSI typing in the future.
2019-09-04 | PXD013980 | Pride
Project description:The overall goal of this project is to investigate the role of TGF-beta signaling in palate development in order to discover candidate therapeutics for preventing and treating congenital birth defects. Here, we conducted gene expression profiling of embryonic palatal tissue from wild type mice as well as those with a neural crest specific conditional inactivation of the Tgfbr2 gene. The latter mice provide a model of cleft palate formation. To investigate the mechanism of cleft palate resulting from mutations in TGFBR2, we analyzed neural crest specific conditional inactivation of Tgfbr2 in mice (Tgfbr2fl/fl;Wnt1-Cre). We performed microarray analyses using the palatal tissue of Tgfbr2fl/fl;Wnt1-Cre mice at embryonic day E13.5 (prior to palatal fusion, n=6 per genotype) and E14.5 (during palatal fusion, n=5 per genotype) to examine the genes regulated by Tgf-beta during palate formation.
2011-11-29 | E-GEOD-22989 | biostudies-arrayexpress
Project description:The overall goal of this project is to investigate the role of TGF-beta signaling in palate development in order to discover candidate therapeutics for preventing and treating congenital birth defects. Here, we conducted gene expression profiling of embryonic palatal tissue from wild type mice as well as those with a neural crest specific conditional inactivation of the Tgfbr2 gene. The latter mice provide a model of cleft palate formation.
2011-11-29 | GSE22989 | GEO
Project description:Transforming growth factor beta receptor 2 (Tgfbr2) was predicted as a causal gene for abdominal using a novel statistical method named LCMS (Schadt et al., 2005, Nature Genetics). In order to validate this prediction, we profiled the liver tissues of Tgfbr2 heterozygous knockout mice (Tgfbr2+/-) and their littermate wild-type (wt) controls to examine the gene expression signature as well as pathways/networks resulting from the single gene perturbation.
2009-03-08 | GSE11994 | GEO