Examining efficiency of enrichment of kidney pericyte-specific messages by TRAP (Translating Ribosome Affinity Purification)
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ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: GUDMAP Developers
PROVIDER: E-GEOD-50439 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:The long term goal is to define the transcriptional changes that accompany pericyte-to-myofibroblast transition in fibrotic kidney disease. Medullary pericytes are identified by their expression of a eGFPL10a fusion protein whose expression is driven by a Col1a1 promoter. Pericyte-specific RNA is generated by eGFP-affinity purification of polysomes from medullary lysates and then subject to microarray analysis.
2014-03-01 | GSE50439 | GEO
Project description:The long term goal is to create an encyclopaedia of podocyte gene expression both in homeostasis, development and disease. Podocytes are identified by their expression of an eGFPL10a fusion protein whose expression is driven by a Col1a1 promoter fragment. Podocyte-specific RNA is generated by eGFP-affinity purification of polysomes and then subject to microarray analysis. Expression profiling of wild type and Actinin 4 point mutant knock-in kidney podocytes by TRAP. Col1a1-eGFPL10a mice were crossed against Actn4+/tm1.1Plk (KI) mice. Wild-type or KI mice were subject to TRAP at the following time points: 2, 5 and 44 weeks.
2014-02-01 | E-GEOD-53156 | biostudies-arrayexpress
Project description:Proteomics analysis can reveal the differences of protein expression between mural cells (known as pericytes) from normal adjacent tissues (NPC) and tumors (TPC), implying the effectiveness of pericyte to tumor.
2021-08-24 | PXD026963 | Pride
Project description:We created a rat renal congestion model and investigated the effect of renal congestion on hemodynamics and molecular mechanisms. The inferior vena cava (IVC) between the renal veins was ligated by suture in male Sprague-Dawley rats to increase upstream IVC pressure and induce congestion in the left kidney only. Left kidney congestion reduced renal blood flow, glomerular filtration rate, and increased renal interstitial hydrostatic pressure. Tubulointerstitial and glomerular injury and medullary thick ascending limb hypoxia were observed only in the congestive kidneys. Molecules related to extracellular matrix expansion, tubular injury, and focal adhesion were upregulated in microarray analysis. Renal decapsulation ameliorated the tubulointerstitial injury. Electron microscopy captured pericyte detachment in the congestive kidneys. Transgelin and platelet-derived growth factor receptors, as indicators of pericyte-myofibroblast transition, were upregulated in the pericytes and the adjacent interstitium. With the compression of the peritubular capillaries and tubules, hypoxia and physical stress induce pericyte detachment, which could result in extracellular matrix expansion and tubular injury in renal congestion.
2018-11-14 | GSE114031 | GEO
Project description:Background: Pericytes regulate vessel stabilization and function and their loss is associated with diseases such as diabetic retinopathy or cancer. Despite their physiological importance, pericyte function and molecular regulation during angiogenesis remain poorly understood. Methods: To decipher the transcriptomic programs of pericytes during angiogenesis, we crossed the Pdgfrb(BAC)-CreERT2 into the RiboTagflox/flox mice. Pericyte morphological changes were assessed in mural cell-specific R26-mTmG reporter mice, in which low doses of tamoxifen allowed labeling of single cell pericytes at high resolution. To study the role of phosphoinositide 3-kinase (PI3K) signaling in pericyte biology during angiogenesis, we used genetic mouse models which allow selective inactivation of PI3Kα and PI3Kβ isoforms and their negative regulator PTEN (phosphate and tensin homologue deleted on chromosome ten, PTEN) in mural cells. Results: At the onset of angiogenesis, pericytes exhibit molecular traits of cell proliferation and activated PI3K signaling, whereas during vascular remodeling pericytes upregulate genes involved in mature pericyte cell function, together with a remarkable decrease in PI3K signaling. Immature pericytes showed stellate shape and high proliferation, and mature pericytes were quiescent and elongated. Unexpectedly, we demonstrate that the PI3Kβ, but not PI3Kα, regulates pericyte proliferation and maturation during vessel formation. Genetic PI3Kβ inactivation in pericytes triggered early pericyte maturation. Conversely, unleashing PI3K signaling by means of PTEN deletion delayed pericyte maturation. Pericyte maturation was necessary to undergo vessel remodeling during angiogenesis. Conclusions: Our results identify new molecular and morphological traits associated to pericyte maturation and uncover PI3Kβ activity as a checkpoint to ensure appropriate vessel formation. In turn, our results may open new therapeutic opportunities to regulate angiogenesis in pathological processes through the manipulation of pericyte PI3Kβ activity.
2020-06-03 | GSE131534 | GEO
Project description:Circular RNAs (circRNAs) are generated by back-splicing and control cellular signaling and phenotypes. Pericytes stabilize the capillary structure and play an important role in the formation and maintenance of new blood vessels. Here, we characterized hypoxia-regulated circRNAs in human pericytes and showed that circPLOD2 is induced by hypoxia and regulates pericyte functions. Silencing of circPLOD2 increased pericyte proliferation, endothelial-pericyte interactions and tube formation. Transcriptional profiling of circPLOD2-depleted cells and epigenomic analyses revealed widespread changes in gene expression and identified the regulation of the transcription factor KLF4 as a key effector of these changes. Importantly, overexpression of KLF4 was sufficient to reverse the effects on pericyte proliferation and endothelial-pericyte interactions observed after circPLOD2 depletion. Together, these data reveal a novel function of circPLOD2 in the control of pericyte proliferation and capillary formation and show that circPLOD2-mediated regulation of KLF4 significantly contributes to the transcriptional response to hypoxia.
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Project description:Pericytes are essential for vessel maturation and endothelial barrier function. Long non-coding RNAs (lncRNAs) regulate endothelial cell function, but their role in pericyte biology remains unexplored. Here we characterize the human pericyte transcriptome following knockdown of lncRNA HypERrlnc (RP11-65J21.3).
2017-08-10 | GSE92887 | GEO
Project description:HiC experiment done on brain pericyte For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
2017-10-23 | GSE105513 | GEO
Project description:The blood-brain barrier (BBB) consists of specific physical barriers, enzymes and transporters, which together maintain the necessary extracellular environment of the central nervous system (CNS). The main physical barrier is found in the CNS endothelial cell, and depends on continuous complexes of tight junctions combined with reduced vesicular transport. Other possible constituents of the BBB include extracellular matrix, astrocytes and pericytes, but the relative contribution of these different components to the BBB remains largely unknown. Here we demonstrate a direct role of pericytes at the BBB in vivo. Using a set of adult viable pericyte-deficient mouse mutants we show that pericyte deficiency increases the permeability of the BBB to water and a range of low-molecular-mass and high-molecular-mass tracers. The increased permeability occurs by endothelial transcytosis, a process that is rapidly arrested by the drug imatinib. Furthermore, we show that pericytes function at the BBB in at least two ways: by regulating BBB-specific gene expression patterns in endothelial cells, and by inducing polarization of astrocyte end-feet surrounding CNS blood vessels. Our results indicate a novel and critical role for pericytes in the integration of endothelial and astrocyte functions at the neurovascular unit, and in the regulation of the BBB. The brain microvascular fragments were isolated from mice with different genotypes, each represented by 3-4 biological replicates. Genotypes 1-2: Platelet derived growth factor-B (PDGF-B) retention-motif knockout (pdgfbret/ret) represent the pericyte-deficient situation, and the heterozygous mice (pdgfbret/+) are used as controls. Genotypes 3-4: Hypomorphic PDGF-B mutants that rescue pdgfb-/- null mice, in which a one copy of a conditionally silent human PDGF-B transgene targeted to the Rosa 26 locus (R26P) is turned on by endothelial-specific expression of Cre recombinase. In this data set these mice are named as Tie2Cre, R26P+/0, pdgfb-/- (representing the pericyte-deficient situation). Mice wt for pdgfb (pdgfb+/+) and carrying one silent copy of R26P (R26P+/0), are used as controls. Genotype 5: Adult Notch3+/+ wildtype (WT).
2010-10-21 | E-GEOD-15892 | biostudies-arrayexpress
Project description:Pericytes and endothelial cells (ECs) are building blocks of blood vessels. While the contributions of ECs to tumor angiogenesis and the tumor microenvironment are well established and multiple drugs that targeting ECs have been developed for clinic use to treat cancers, the underlying mechanisms of pericyte in supporting tumor vessel and in shaping tumor microenvironment remains largely unexplored and no pericyte targeting strategies have been approved yet. This study employs targeted deletion of the NO receptor sGC in pericytes and utilizes single-cell RNA sequencing to elucidate its impact on the tumor microenvironment. The results unveil a disruptive effect on EC-pericyte interactions, subsequently impeding Notch-mediated intercellular crosstalk and prompting extensive transcriptomic reprogramming in both cell types. This vascular alteration further relays to neighboring cancer-associated fibroblasts (CAFs) and tumor-associated macrophages (TAMs) through paracrine signaling, collectively suppressing tumor growth. Importantly, the inhibition of pericyte sGC has limited influence on quiescent vessels but significantly sensitizes angiogenic vessels to anti-angiogenic treatment. In conclusion, this study underscores the vital role of pericytes in governing tumor vessels and the tumor microenvironment, suggesting that targeting pericyte sGC holds promise for enhancing anti-angiogenic therapy.
2024-02-01 | GSE243313 | GEO