Comparative expression data from HBVP (human brain vascular pericytes) and human MSC (mesenchymal stem cells)
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE46235 | GEO | 2013/12/04
SECONDARY ACCESSION(S): PRJNA198272
REPOSITORIES: GEO
Similar Datasets
Project description:Pericytes and mesenchymal stem cells (MSC) are ontogenically related, and in fact no phenotypic differences were observed by flow cytometry using a panel of surface antigen markers. Global gene expression profiles of human pericytes and MSC revealed that 43 genes were expressed more than 10 fold in pericytes as compared to MSC. Cells were cultured in 24-w plates in complete medium for 24h in biological triplicates
2013-12-04 | E-GEOD-46235 | biostudies-arrayexpress
Project description:Identification of TLR4 as one of the most abundant RNA species in pericytes with respect to MSC, and corroboration of TLR4 expression on the cell surface, led us to obtain a comprehensive overview of the expression program of lipopolysaccharide (LPS) stimulated pericytes. Microarray analyisis demonstrated the significant upregulation of 76 annotated genes including transcripts for adhesion molecules, inflammation mediators, pro-angiogenic factors, transcription factors and anti-apoptotic proteins. Cells were cultured in 24-w plates in complete medium for 24h before stimulation with 1 microgram/ml LPS for 4h. Samples are biological triplicates.
2013-12-04 | E-GEOD-46236 | biostudies-arrayexpress
Project description:Identification of TLR4 as one of the most abundant RNA species in pericytes with respect to MSC, and corroboration of TLR4 expression on the cell surface, led us to obtain a comprehensive overview of the expression program of lipopolysaccharide (LPS) stimulated pericytes. Microarray analyisis demonstrated the significant upregulation of 76 annotated genes including transcripts for adhesion molecules, inflammation mediators, pro-angiogenic factors, transcription factors and anti-apoptotic proteins.
2013-12-04 | GSE46236 | GEO
Project description:Transcriptomics signature of human heart vascular pericytes
| PRJNA802679 | ENA
Project description:Pericytes/vascular smooth muscle cells (VSMCs), regulated by platelet-derived growth factor receptor β (PDGFRβ) signaling, play important roles in endothelial survival and vascular stability. Here we report that treatment with imatinib, an inhibitor of PDGFRβ, led to significant tumor growth impairment associated with increased apoptosis in human lymphoma xenografts including Farage, Karpas422 and OCI-Ly7 in SCID mice. Confocal analysis of the tumor tissue showed decreased microvessel density, decreased vascular flow, and increased vascular leak in the imatinib-treated cohorts. Imatinib targeted tumor-associated PDGFRβ+ pericytes in vivo by inducing apoptosis and disruption of the PDGFRβ+ perivascular network, and PDGFRβ+ VSMC in vitro by inhibition of proliferation. FACS analysis of mononuclear cell suspension of tumor tissues revealed decreased mature pericytes and endothelial cells, as well as their progenitors with imatinib treatment. Compared to imatinib, treatment with anti-PDGFRβ monoclonal antibody partially inhibited the growth of Farage lymphomas. Lastly, microarray analysis of differentially expressed genes in PDGFRβ+ VSMC following imatinib treatment showed significant down-regulation of genes implicated in proliferation, survival and angiogenesis, including those within PI3K/AKT and MAPK/ERK1/2 pathways downstream of PDGFRβ signaling. Taken together, targeting PDGFRβ+ pericytes in lymphoma presents a novel and complementary target to endothelial cells for efficacious antiangiogenic therapy. PDGFRb+ murine vascular smooth muscle cells (VSMCs) were treated in 10 uM imatinib for 24 or 48 hours. Gene expression changes in response to imatinib treatment were examined using NimbleGen MM8_60mer gene expression microarrays by comparing expression patterns at 24- and 48-hours treatment to the baseline level (0 hours).
2013-04-22 | E-GEOD-30752 | biostudies-arrayexpress
Project description:Pericytes (PC) are abundant yet remain the most enigmatic and ill-defined cell population in the heart. Here, we investigated whether PC can be reprogrammed to aid neovascularisation of the heart post-myocardial infarction. We discovered that culture of human cardiac PC for 10 days in the presence of an inhibitor of ERK1/2 signalling (PD0325901, specific MEK1/2 inhibitor) induces the PC switch towards a vascular smooth muscle cells (VSMC)-like phenotype. Differentiated PC became more proangiogenic, more responsive to vasoactive agents, and insensitive to chemoattractants. RNA-Sequencing revealed transcripts marking the PD0325901-induced transition into proangiogenic, stationary VSMC-like cells.
2022-03-29 | GSE195917 | GEO
Project description:Brain perivascular cells have been recently identified as new mesodermal cell type of the human brain. These cells reside in the perivascular niche and were shown to have mesodermal and â to a lesser extend â tissue-specific differentiation potential. Mesenchymal stem cells (MSCs) are widely discussed for the use in cell therapy in many neurological disorders. Therefore it is of importance to better understand the âintrinsicâ MSC population of the human brain. Here we systematically characterized adult human brain-derived pericytes during in vitro expansion and differentiation and compared these cells to fetal and adult human brain-derived NSCs and adult human bone marrow derived MSCs. We found that adult human brain pericytes can be isolated from hippocampal as well as cortical white matter, are â in contrast to adult human NSCs â easily expandable in monolayer cultures and show high similarities to human bone marrow-derived MSCs both regarding surface marker expression and whole transcriptome analysis. Human brain pericytes differentiated only in negligible amounts into neuroectodermal cell types using various differentiation conditions but efficiently differentiated into mesodermal progenies. Thus bone marrow-derived MSCs resemble human brain pericytes and might be therefore very interesting for possible autologous NPC-based treatment strategies, cell therapeutic approaches of neurological diseases. For the gene expression microarray analysis we used the Affymetrix U133A chips The whole procedure was performed following the manufacturer's standard protocol (Affymetrix, Santa Clara, CA). For the data processing, normalization was calculated with the GCRMA (GC content corrected Robust Multi-array Analysis) algorithm. Data post-processing and graphics was performed with in-house developed functions in Matlab. 17 samples were analyzed fNSC, Neural Stem Cell, 2 replicates ANPC-hip, adult Neuroprogenitor - Cell Hippocampus, 3 replicates ANPC-wm, adult Neuroprogenitor Cell - White Matter, 3 replicates ABPMC-hip, adult Brain Perivascular Mesodermal Cell - Hippocampus, 3 replicates ABPMC-wm, adult Brain Perivascular Mesodermal Cell - White Matter, 3 replicates MSC, Mesenchymal Stem Cell, 3 replicates
2015-11-03 | E-GEOD-62505 | biostudies-arrayexpress
Project description:Pericytes/vascular smooth muscle cells (VSMCs), regulated by platelet-derived growth factor receptor β (PDGFRβ) signaling, play important roles in endothelial survival and vascular stability. Here we report that treatment with imatinib, an inhibitor of PDGFRβ, led to significant tumor growth impairment associated with increased apoptosis in human lymphoma xenografts including Farage, Karpas422 and OCI-Ly7 in SCID mice. Confocal analysis of the tumor tissue showed decreased microvessel density, decreased vascular flow, and increased vascular leak in the imatinib-treated cohorts. Imatinib targeted tumor-associated PDGFRβ+ pericytes in vivo by inducing apoptosis and disruption of the PDGFRβ+ perivascular network, and PDGFRβ+ VSMC in vitro by inhibition of proliferation. FACS analysis of mononuclear cell suspension of tumor tissues revealed decreased mature pericytes and endothelial cells, as well as their progenitors with imatinib treatment. Compared to imatinib, treatment with anti-PDGFRβ monoclonal antibody partially inhibited the growth of Farage lymphomas. Lastly, microarray analysis of differentially expressed genes in PDGFRβ+ VSMC following imatinib treatment showed significant down-regulation of genes implicated in proliferation, survival and angiogenesis, including those within PI3K/AKT and MAPK/ERK1/2 pathways downstream of PDGFRβ signaling. Taken together, targeting PDGFRβ+ pericytes in lymphoma presents a novel and complementary target to endothelial cells for efficacious antiangiogenic therapy.
2013-04-22 | GSE30752 | GEO
Project description:Tumor necrosis factor alpha induces vascular permeability, playing an important role in inflammation. Also, TNF-induced vascular leakage is involved in the increased extravasation of nanoparticle formulated chemotherapeutics improving drug delivery and subsequently tumor response, and we found a positive correlation between the presence of pericytes in the tumor-associated vasculature and TNF-induced leakage. RNA sequencing and pathway analysis of TNF-stimulated versus non-stimulated pericytes and endothelial cells show significant upregulation of several pathways involving interferon regulating pathways with a high expression of CXCL10, also known as Interferon gamma-inducible protein 10 (IP-10) in TNF-stimulated pericytes. In addition, CXCL10 protein production was significantly increased in conditioned medium from TNF-exposed pericytes compared to the other conditions. In our animal studies, we observed that tumor types with high pericyte covered vessels show enhanced permeability when exposed to TNF, which can be blocked with a neutralizing CXCL10 antibody. Vice versa, tumors with vessels low in pericyte number do not respond to TNF, i.e., do not express elevated permeability. Importantly, this lack of pericyte coverage can be compensated by co-administration of CXCL10. Our finding reveals a mechanism where TNF induces CXCL10 release from pericytes, being at the basis of increased permeability and thus vascular leakage.
2022-07-01 | GSE203505 | GEO
Project description:The objective of this array was to determine the global gene expression profile of human placental pericytes for comparison with other publicly available arrays of pericytes and mesenchymal stromal cells isolated from various human tissues. Pericytes are critical cellular components of the microvasculature that play a major role in vascular development and pathologies, yet their study has been hindered by lack of a standardized method for their isolation and growth. Here we report a method for culturing human pericytes from a readily available tissue source, placenta, and provide a thorough characterization of resultant cell populations. We developed an optimized protocol for obtaining pericytes by outgrowth from microvessel fragments recovered after enzymatic digestion of human placental tissue. We characterized outgrowth populations by immunostaining, by gene expression analysis, and by functional evaluation of cells implanted in vivo. Our approach yields human pericytes that may be serially expanded in culture and that uniformly express the cellular markers NG2, CD90, CD146, α-SMA, and PDGFR-β, but lack markers of smooth muscle cells, endothelial cells, and leukocytes. When co-implanted with human endothelial cells into C.B-17 SCID/bg mice, human pericytes invest and stabilize developing human endothelial cell-lined microvessels. We conclude that our method for culturing pericytes from human placenta results in the expansion of functional pericytes that may be used to study a variety of questions related to vascular biology. Total RNA from three different pericyte isolations at subculture 1 was collected and examined for relative gene expression.
2010-04-14 | E-GEOD-21332 | biostudies-arrayexpress