Expression data from mouse microvascular transcriptomes
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE9202 | GEO | 2008/09/27
SECONDARY ACCESSION(S): PRJNA102783
REPOSITORIES: GEO
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Project description:Little is known about the pan-microvascular transcriptome, particularly considering gene transcripts and their encoded proteins that can be considered as vascular-selective in their expression. Using a combination of publicly available and our own transcript profiles, we identified a core set of gene transcripts, which are specifically and broadly expressed in the microvasculature. Experiment Overall Design: There are three different samples, each have three biological repeats. Comparisons were carried out between the samples.
2008-10-26 | E-GEOD-9202 | biostudies-arrayexpress
Project description:The microvasculature plays a key role in tissue perfusion, transport of mediators, and exchange of gases and metabolites to and from tissues. Microvascular dysfunction has emerged as an important contributor to cardiovascular diseases. In this study we used human blood vessel organoids (BVOs) as a model of the microvasculature to delineate the mechanisms of microvascular dysfunction caused by metabolic rewiring. BVOs fully recapitulated key features of the normal human microvasculature, including reliance of mature endothelial cells (ECs) on glycolytic metabolism, as concluded from metabolic flux assays using 13C-glucose labelling and mass spectrometry-based metabolomics. Pharmacological targeting of PFKFB3, a potent activator of glycolysis, with two different chemical inhibitors resulted in rapid BVO restructuring, vessel regression with reduced pericyte coverage. PFKFB3 mutant BVOs also displayed similar structural remodelling compared to control BVOs. Proteomic analysis of the BVO secretome revealed remodelling of the extracellular matrix and differential expression of paracrine mediators such as CTGF. Treatment with recombinant CTGF recovered tight junction formation and increased pericyte coverage in microvessels. Our metabolic and proteomics findings demonstrate that BVOs rapidly undergo restructuring in response to metabolic changes and identify CTGF as a critical paracrine regulator of microvascular integrity.
2023-09-13 | PXD041780 | Pride
Project description:The placental microvasculature of the human fetus is essential for the efficient transfer of gases, nutrients and waste between the mother and fetus. Microvascular hypoplasia of the terminal villi is associated with the placental pathology observed in cases of severe Intra Uterine Growth Restriction (IUGR). We used novel methods to isolate a pure population of placental microvascular endothelial cells from control preterm placentas (n=3) and placenta complicated by severe IUGR (n=6) with superimposed preeclampsia (n=5). Distal placental villous tissue was collected to enrich for terminal villi. Tissue was minced, digested and placental microvascular endothelial cells (PlMEC) were positively selected using tocosylated magnetic Dynabeads labeled with Human Endothelial Antigen lectin. The purity of the PlMEC (95%) was assessed by CD31 immunocytochemistry. RNA was extracted from the PlMEC samples and also from 3 term placenta and subjected to Affymetrix microarray analysis (U133Plus2 array chips). Data from the 3 term placentas and 3 preterm PlMEC arrays was used to generate an endothelial cell specific gene profile. This profile was used to identify the endothelial genes differentially regulated in all 6 IUGR cases. BTNL9 and NTRK2 transcripts were upregulated and SAA1, GNAS and SLAMF1 transcripts were downregulated as relative to the preterm controls. These changes were validated by Real time PCR in the PlMEC samples. This novel study is the first to identify endothelial candidate genes that may play a role in the villous hypoplasia of severe IUGR. This work advances our understanding of the molecular defects in placental microvascular endothelial cells in normal and pathologic pregnancies.
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2016-10-24 | E-GEOD-75668 | biostudies-arrayexpress
Project description:Purpose: Pericytes, the mural cells of blood microvessels, have come into focus as regulators of microvascular development and function, but due to paucity of defining markers, the identification and functional characterization of PC remain problematic, and reported data are often controversial. Here, we used a new approach for the isolation of mural cell from mouse brain in combination with RNA-sequencing (RNA-seq) and previously published vascular transcriptome data to assemble a state-of-the-art catalogue of brain mural cell-enriched gene transcripts. Methods: We isolated double positive cells from the brain of Pdgfrb-eGFP/NG2-DsRed transgenic mice using FACS. Cells were lysed, RNA extracted and sequenced with next-generation sequencing (NGS). For comparison, we also determined the transcriptome of brain microvascular fragments (containing both endothelial cells and mural cells) isolated by mechanical tissue disintegration, collagenase digestion and immune-panning using anti-CD31 antibodies coupled to magnetic beads. The reads were aligned to the Ensembl mouse gene assembly (NCBIM37) using Tophat2 software (version 2.0.4). The duplicated reads were removed using the picard tool (version 1.92). To identify the genes significantly enriched in the pericyte samples as compared with microvascular samples, statistical tests were performed using the Cufflinks tool (version 2.2.1) Results: The result showed that mRNA transcripts representing 856 different genes were enriched more than two-fold in FACS isolated Pdgfrb-eGFP/NG2-DsRed double positive cells compared with whole microvascular fragments (False Discovery Rate < 0.05)
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Project description:In this study, we examined the impact of modulating the TGF-β/PAI-1 axis in CD34+ cells function from diabetic patients and controls. Using gene array studies, we found that diabetics, protected from microvascular complications despite suboptimal glycemic control, had reduced level of TGF- β1 and PAI-1 transcripts in their CD34+ cells compared to age, sex, duration and degree of glycemic control -matched diabetics with microvascular complications. Treatment with neutralizing antibody to TGF- β1 in murine hematopoietic stem cells (HSC) enhanced in vivo repopulation potential of these cells in bone marrow transplantation; reduced the time required for cell division of single cells, increased survival of the progenitor cells and reduced TGF-β1 expression. TGF- β1 phosphorodiamidate morpholino oligomers (PMO) treatment reduced PAI-1 mRNA expression in diabetic (p<0.01) and non-diabetic (p=0.05) CD34+ cells. Inhibition of PAI-1 promoted CD34+ cell proliferation and migration in vitro.Targetting TGFβ-1/PAI-1 system offers a promising therapeutic strategy for restoring vascular reparative function in diabetic CD34+ cells and hematopoietic stem cells, enhancing key functions needed for cell therapy. Peripheral blood from either age matched controls (n=5), diabetics with long standing poorly controlled diabetes and no microvascular complications (n=4), and diabetics with long-standing poorly controlled diabetes with severe microvascular complications (n=5) was obtained and CD34+ cells were isolated. RNA was extracted followed by AffyNugen amplification, and the cDNA was probed to Human RSTA Affymetrix 2.0 chip
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