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Gene expression profile of endothelial cells maturated into brain-like endothelial cells

ABSTRACT: To understand the molecular mechanisms during the maturation of cord blood-derived endothelial cells into blood brain barrier capillary endothelial cells (BCECs), we have employed whole genome microarray expression profiling to identify genes responsible for the maturation process. Hematopoietic stem cells were isolated from cord-blood samples and differentiated into endothelial cells. The endothelial cells were further maturated into BCECs by co-culturing with blood-brain barrier (BBB) specific cells (pericytes) for 3 days and 6 days.

ORGANISM(S): Homo sapiens

PROVIDER: GSE45171 | GEO | 2013/10/18

SECONDARY ACCESSION(S): PRJNA193225

REPOSITORIES: GEO

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Gene expression profile of endothelial cells maturated into brain-like endothelial cells

Project description:To understand the molecular mechanisms during the maturation of cord blood-derived endothelial cells into blood brain barrier capillary endothelial cells (BCECs), we have employed whole genome microarray expression profiling to identify genes responsible for the maturation process. Hematopoietic stem cells were isolated from cord-blood samples and differentiated into endothelial cells. The endothelial cells were further maturated into BCECs by co-culturing with blood-brain barrier (BBB) specific cells (pericytes) for 3 days and 6 days. The gene expression in human hematopoietic stem cell-derived endothelial cells was measured at 3 and 6 days after co-culture with pericytes. Three independent experiments were performed at each time (3 or 6 days). The RNA obtained from different experiments were pooled together for each group before microarray studies.

2013-10-18 | E-GEOD-45171 | biostudies-arrayexpress

Comparative genomic hybridization by array of rat brain- and spinal cord-derived microvascular endothelial cells, in basal and inflammatory conditions upon different time points of TNF-Î±-treatment or TWEAK-treatment or LPS-treatment.

Project description:The brain and spinal cord are endowed with particular vascular systems, known as the blood-brain barrier (BBB) and blood-spinal cord barrier (BSCB) respectively, which maintain homeostasis between nervous parenchyma and peripheral circulation. Despite these common features, the BSCB presents structural and functional differences resulting in distinct vulnerability to pathological insults when compared to the BBB. Although, the heterogeneity of endothelial cell types underlies their remarkable ability to sub-specialize and provide specific requirements for a given vascular bed, very little is known concerning intrinsic differences between microvascular endothelial cells (MECs) derived from brain (BMECs) and spinal cord (SCMECs), including their response to inflammation. We used Agilent Whole Rattus Genome Microarray 4X44K to compare rat BMECs and SCMECs in both basal and inflammatory conditions; TNF-Î±-induced, TWEAK-induced and LPS-induced gene expression after 6 hr, 12 hr, 24 hr and 48 hr incubation.

2016-06-20 | E-MTAB-4696 | biostudies-arrayexpress

RNA-seq of human primary endothelial cells

Project description:Endothelial cells represent the key cellular components of the blood-brain barrier, whose selective permeability presents a challenge for drug delivery. A better understanding of molecular proteins specific for brain endothelial cells compared to endothelial barries in different tissues can highlight novel blood-brain barrier transport targets.

2023-03-08 | GSE226605 | GEO

An organ-specific angiogenic control mechanism for endothelial tailoring.

Project description:Each organ of the human body requires locally-adapted blood vessels1–3. The gain of such organotypic vessel specializations is often deemed molecularly unrelated to the process of organ vascularization. Opposing this model, we reveal a molecular mechanism for brain-specific angiogenesis that operates under the control of Wnt7a/b ligands, well-known blood-brain barrier maturation signals4–6. The control mechanism relies on Wnt7a/b-dependent expression of Mmp25 in brain endothelial cells. This hitherto poorly characterized GPI-anchored matrix metalloproteinase is selectively required in endothelial tip cells to enable their initial migration across the pial basement membrane which lines the brain surface, and whose distinctive molecular composition is controlled by embryonic pial fibroblasts. Mechanistically, Mmp25 confers brain invasive competence by cleaving the pial basement membrane-enriched Col4a5/6 within a short non-collagenous region of the central helical part of the heterotrimer. Upon genetic interference with pial basement membrane composition, the Wnt/β-catenin-dependent organotypic control of brain angiogenesis is lost, resulting in a properly patterned, yet blood-brain barrier-defective cerebrovasculature. This work reveals an organ-specific angiogenesis mechanism, sheds light on tip cell mechanistic angiodiversity, and thereby illustrates how organs, by imposing local constraints on angiogenic tip cells, can select vessels matching their distinctive physiological requirements.

2024-02-08 | PXD042613 | Pride

An organ-specific angiogenic control mechanism for endothelial tailoring

Project description:Each organ of the human body requires locally-adapted blood vessels. The gain of such organotypic vessel specializations is often deemed molecularly unrelated to the process of organ vascularization. Opposing this model, we reveal a molecular mechanism for brain-specific angiogenesis, that operates under the control of Wnt7a/b ligands, well-known blood-brain barrier maturation signals. The control mechanism relies on Wnt7a/b-dependent expression of Mmp25 in brain endothelial cells. This hitherto poorly characterized GPI-anchored matrix metalloproteinase is selectively required in endothelial tip cells to enable their initial migration across the pial basement membrane lining the brain surface, which distinctive molecular composition is controlled by embryonic pial fibroblasts. Mechanistically, Mmp25 confers brain invasive competence by cleaving the pial basement membrane-enriched Col4a5/6 within a short non-collagenous region of the central helical part of the heterotrimer. Upon genetic interference with pial basement membrane composition, the Wnt/β-catenin-dependent organotypic control of brain angiogenesis is lost, resulting in properly patterned, yet blood-brain barrier-defective cerebrovasculatures. This work reveals an organ-specific angiogenesis mechanism, sheds light on tip cell mechanistic angiodiversity, and thereby illustrates how organs, by imposing local constraints on angiogenic tip cells, can select vessels matching their distinctive physiological requirements.

2024-02-08 | GSE233662 | GEO

The effect of corticosterone treatment on the proteome of mouse brain endothelial bEnd.3 cells

Project description:Elevated glucocorticoids feature body’s responses to a variety of psychological and physiological stressors. To understand how glucocorticoids affect brain endothelial cells that form the blood-brain barrier, we applied quantitative proteomics to study changes in the proteome of a mouse brain endothelial cell line, bEnd3, upon acute 24-hour treatment with 5 uM corticosterone in vitro.

2021-03-01 | PXD022166 | Pride

Gene expression data from mouse brain endothelial cells after SAH

Project description:SAH pathophysiology includes blood-brain barrier (BBB) disruption. Gene expression changes at the endothelial cell level may provide insight into BBB pathophysiology. We used microarray gene expression data comparing freshly isolated brain endothelial cells isolated from Sham or SAH mice.

2021-04-12 | GSE155137 | GEO

Brain microvascular endothelial cells: INSR KD

Project description:The insulin receptor (INSR) mediates insulin signaling to modulate cellular functions. Although INSR is expressed at the blood-brain barrier (BBB), its role in the modulation of BBB function is poorly understood. Therefore, in this study, we aimed to analyze the effect of INSR knockdown on the expression levels of functional proteins at the BBB. We established the INSR-knockdown cell line (shINSR) using human cerebral microvascular endothelial cells (hCMEC/D3). The cellular proteome was analyzed using quantitative proteomics. Protein expression levels were quantified by targeted proteomics.

2021-12-25 | PXD027326 | JPOST Repository

CRISPR/Cas9 genome editing demonstrates that CCM3 modulates endothelial miRNA expression

Project description:CCM3 regulates blood-brain-barrier integrity and vascular maturation in vivo. CCM3 loss-of-function variants predispose to cerebral cavernous malformations (CCM). Various signalling pathways are deregulated upon CCM3 depletion in endothelial cells (ECs). In this study, we established a crRNA:tracrRNA:Cas9 RNP approach to efficiently knockout CCM3 in human ECs and studied the molecular and functional effects of its long-term inactivation. Using small RNA sequencing, we show that CCM3 regulates the expression of aging‑associated miRNAs.

2019-01-18 | GSE114947 | GEO

Expression data of E13.5 mouse Blood Brain Barrier and lung endothelial cells

Project description:Following the identification of a critical time window of Blood Brain Barrier formation in the mouse embryo, we aimed to identify genes important for barriergenesis. To this end, we isolated cortical and lung E13.5 endothelial cells and compared expression between the two populations. The working hypothesis was that endothelial cells which are actively building a barrier would have a uniqe pattern of gene expression that would be detectable in comparison to a non-barrier endothelial population that is also active in vasculogenesis. E13.5 Tie2-GFP embryos were micro-dissected for cortex and lungs. Cortex tissue was carefully cleared of the meninges and choroid plexus. FACS purification of GFP positive cells and GeneChip analysis was applied . All material from a single litter (10-13 embryos) was pooled and considered as a biological replicate. n=4 litters.

2014-05-14 | E-GEOD-56777 | biostudies-arrayexpress

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