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Expression data from adult lungs isolated from TMEM100-deficient mice

ABSTRACT: Tmem100 was identified as a downstream gene of BMP9-ALK1 signaling. The signaling has been implicated in hereditary hemorrhagic telangiectasia. This study was designed to identify affected genes in TMEM100-deficiect mice. Tmem100 was inactivated in adult Tmem1002loxP/2loxP;ROSA26+/CreER mice by tamoxifen tereatment. Microarray data was obtained from the lungs isolated from tamoxifen treated control and mutant mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE57256 | GEO | 2014/05/03

SECONDARY ACCESSION(S): PRJNA246087

REPOSITORIES: GEO

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Expression data from adult lungs isolated from TMEM100-deficient mice

Project description:Tmem100 was identified as a downstream gene of BMP9-ALK1 signaling. The signaling has been implicated in hereditary hemorrhagic telangiectasia. This study was designed to identify affected genes in TMEM100-deficiect mice. Tmem100 was inactivated in adult Tmem1002loxP/2loxP;ROSA26+/CreER mice by tamoxifen tereatment. Microarray data was obtained from the lungs isolated from tamoxifen treated control and mutant mice. Three control mice (Tmem1002loxP/2loxP) and three mutant mice (Tmem1002loxP/2loxP;ROSA26+/CreER) were treated with tamoxifen (two consecutive intraperitoneal injections, 0.1 mg/g of body weight) to activate CreER recombinase. Total RNAs were isolated from lungs 7 days after tamoxifen injection.

2014-05-03 | E-GEOD-57256 | biostudies-arrayexpress

Expression data from BMP9-treated human dermal microvascular endothelial cells (HMVEC-D)

2012-09-19 | GSE40960 | GEO

Expression data from BMP9-treated human dermal microvascular endothelial cells (HMVEC-D)

Project description:BMP9 signaling has been implicated in hereditary hemorrhagic telangiectasia and vascular remodeling, acting via the HHT target genes, endoglin and ALK1. This study sought to identify endothelial BMP9-regulated proteins that could affect the HHT phenotype. Gene ontology analysis of cDNA microarray data obtained following BMP9 treatment of primary human endothelial cells indicated regulation of chemokine, adhesion, and inflammation pathways. The sample set is comprised of three biological replicate control human dermal microvascular endothelial cells, and three treated (5 ng/ml human recombinant BMP9) biological replicate human dermal microvascular endothelial cells

2012-09-19 | E-GEOD-40960 | biostudies-arrayexpress

Deciphering early phosphoproteome changes in response to BMP9 and BMP10 in endothelial cells

Project description:BMP9 and BMP10 are two key regulators of vascular homeostasis. These two ligands bind with high affinity to the endothelial type I receptor ALK1 together with a type 2 receptor. Mutations in this signaling pathway have been identified in two rare cardiovascular diseases, hereditary hemorrhagic telangiectasia and pulmonary arterial hypertension. So far, only the canonical SMAD signaling pathway has been extensively studied in response to BMPs. The aim of this work was to address early phosphoproteomic changes in endothelial cells in response to short-term stimulation (30 mins) with BMP9 and BMP10 in order to identify new phosphorylated targets and signaling pathways.

2024-03-25 | PXD044952 | Pride

Induced Endothelial Cell Cycle Arrest Prevents Arterio-venous Malformations in Hereditary Hemorrhagic Telangiectasia (Bulk RNA-Seq)

Project description:Distinct endothelial cell cycle states (early G1 vs. late G1) provide different “windows of opportunity” to enable the differential expression of genes that regulate venous and arterial specification, respectively. Endothelial cell cycle control and arterial-venous identities are disrupted in vascular malformations including arteriovenous (AV) shunts which is a hallmark of hereditary hemorrhagic telangiectasia (HHT). We show how endothelial cell late G1 arrest induced by Palbociclib modulates the expression of genes regulating arterio-venous identity and prevents AVM development induced by BMP9/10 inhibition.

2023-12-31 | GSE245197 | GEO

Impact of IRP deficiency on the proteome of Ly6G+ cells from the bone marrow in mice

Project description:The overall objective of the project is to evaluate the effects of loss of function of iron regulatory proteins (IRP1, encoded by Aco1)-1 and -2 (IRP2, encoded by Ireb2) during adult life. Mice carrying floxed Aco1 and Ireb2 alleles were crossed to a knockin strain expressing a tamoxifen-inducible CRE recombinase under the control of the Rosa26 promoter. The resulting Aco1flox/flox,Ireb2flox/flox,Rosa26+/CreERT2 mice are designated P1/2-KO; littermates lacking the CreER sequence (Aco1flox/flox,Ireb2flox/flox,Rosa26+/+) serve as reference and are designated P1/2-CTR. Adult mice were injected (i.p.) with tamoxifen on day 1 and day 3 to ablate the IRPs in the whole body, and were sacrificed on day 10 for analysis. Bone marrow cells were collected and LY6G+ cells were magnetically sorted for proteome analysis by LC-MS/MS using an Ultimate 3000 UPLC system connected to an Orbitrap Exploris 480 mass spectrometer.

2023-03-11 | PXD032077 | Pride

Identification of Sox9-Regulated Pathways During the Secondary Transition Stage of Pancreas Development

Project description:Sox9 target genes were identified during the secondary transition stage of pancreas development by comparing gene expression in Sox9-ablated versus wild-type pancreata using microarray analysis. Sox9 was conditionally ablated during the secondary transition in the developing pancreas via recombination of a Sox9-flox allele (Kist et al., 2002) using the tamoxifen-inducible Rosa26-CreER allele (Vooijs et al., 2001). Dams were injected with 6 mg/40 g tamoxifen in corn oil at e12.5. Pancreata were manually microdissected at e15.5. Total RNA was isolated and pooled from pancreata of e15.5 Sox9fl/fl; Rosa26-CreER (mutant) versus Rosa26-CreER (wild-type) littermates for four biological replicates.

2012-08-01 | E-GEOD-28670 | biostudies-arrayexpress

SMAD4 maintains the Fluid Shear Stress set point to protect against Arterial-Venous Malformations

Project description:Vascular networks form, remodel and mature under the influence of both fluid shear stress (FSS) and soluble factors. Physiological FSS promotes and maintains vascular stability via synergy with Bone Morphogenic Protein 9 (BMP9) and BMP10. Conversely, mutation of the BMP receptors ALK1, Endoglin or the downstream effector SMAD4 leads to Hereditary Hemorrhagic Telangiectasia (HHT), characterized by fragile and leaky arterial-venous malformations (AVMs). But how endothelial cells (EC) integrate FSS and BMP signals in vascular development and homeostasis, and how mutations give rise to vascular malformations is not well understood. Here, we aimed to elucidate the mechanism of synergy between fluid shear stress and SMAD signaling in vascular stability and its failure in HHT. We have now found that loss of Smad4 increases ECs’ sensitivity to flow by lowering the FSS set point with resulting AVMs exhibiting features of excessive flow-mediated morphological responses. Mechanistically, loss of Smad4 disinhibits flow-mediated Klf4-Tie2-PI3K/Akt signaling leading to increased EC proliferation and loss of arterial identity due to Klf4-mediated repression of cyclin dependent Kinase (CDK) inhibitors, CDKN2A and CDKN2B. Thus, AVMs caused by Smad4 deletion are characterized by chronic high flow remodeling with excessive EC proliferation and loss of arterial identity as triggering events.

2023-07-03 | GSE232443 | GEO

Project description:A novel mutation gene of Hereditary Hemorrhagic Telangiectasia

| PRJNA781636 | ENA

Transcriptomic data of liver endothelial cells from Alk1-(alias Acvrl1) knockout mice II

Project description:Hereditary hemorrhagic telangiectasia (HHT, alias Rendu-Osler-Weber syndrome) is an autosomal dominant genetic disease that causes vascular malformations in multiple organs. Malformations and shunts in the liver are relevant for the long-term prognosis as they can lead to heart failure. Moreover, the role of ALK-1 in the hepatic vascular niche remains elusive. In this project, we aimed to establish a novel HHT model covering hepatic involvement by the disease and to investigate the role of ALK-1 in the hepatic vascular niche. We crossed Stab2-icre mice (MGI: 6741034) with Acvrl1-floxed mice (MGI: 4398901) to generate constitutive hepatic endothelial Acvrl1 knockout (Acvrl1-HEC-KO, alias Alk1-HEC-KO) mice. To dissect microvascular transcriptomic alterations, we performed RNA sequencing of freshly isolated hepatic endothelial cells from 3 months old mice. Transcriptomic analyses revealed an arterialization of hepatic vessels accompanied by loss of LYVE-1 and induction of Endomucin. The loss of endothelial Wnt2, Wnt9b, and Rspo3 led to a disruption of hepatic metabolic zonation with a dominance of periportal genes in Alk1-HEC-KO mice and HHT patients. Furthermore, we identified PRND (alias Doppel) and placenta growth factor (PlGF) as novel candidates of HHT pathogenesis in mice. ALK-1 controls hepatic metabolic zonation via Wnt signaling and suppresses PRND and PlGF that represent novel candidates in HHT pathogenesis.

2023-04-06 | GSE184747 | GEO

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