ScRNA-seq profiling of vascular cells isolated from disease-free human breast based on the expression of CD36 and/or CD31
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PROVIDER: PRJNA787612 | ENA |
REPOSITORIES: ENA
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Project description:To identify markers preferentially expressed by capillary ECs (highly expressing CD36) in the disease-free human breast and gain insights into their biology, we used single cell RNA sequencing (scRNA-seq). For this analysis, dissociated cells from disease-free tissues were barcoded using the MULTI-seq protocol and pooled prior to FACS-based isolation of CD36+ and/or CD31+ cells. The droplet-based 10x Genomics Chromium platform was used to encapsulate single cells and construct cDNA libraries. Populations of fibroblasts, perivascular, lymphatic and vascular endothelial ECs where identified in this analysis.
2021-12-11 | GSE190592 | GEO
Project description:A major challenge in realizing regenerative treatment using freshly isolated Adipose Derived Regenerative Cells (ADRCs) is the cellular heterogeneity and donor variability. Ex vivo expanded ADRCs (=ASCs) are available at larger quantities and represent a more homogeneous population suitable for allogenic use. Emerging pre-clinical and clinical data however suggest similar, or even superior efficacy of ADRCs as compared to ASCs for indications involving (micro)vascular deficiency. Since CD31+ ADRCs lack in cultured ASCs, we hypothesized that these cells account for improvement of vascular function in the heterogenous ADRCs. Herein, we found that in patients with erectile dysfunction (ED), the number of injected CD31+ ADRCs correlates positively with erectile function 12 months after one bolus of autologous ADRCs. Comprehensive in vitro and ex vivo analyses confirmed superior pro-angiogenic and paracrine effects of human CD31+ enriched ADRCs compared to the corresponding CD31- and parent ADRCs. CD31+, CD31- and ADRCs were co-cultured in aortic ring-, as well as in ED-relevant corpus cavernousum tube formation assays, both showing a significantly higher ability of the CD31+ ADRCs to support tube development. This effect was corroborated using conditioned medium (CM), while quantitative mass spectrometric analysis suggested that this is explained by secretory pro-angiogenic proteins such as DKK3, ANGPT2, ANAX2 and VIM, all being enriched in CD31+ADRC CM. To gain further specification of the ADRC subpopulations expressing these proteins, single-cell RNA sequencing was performed and showed that transcripts of the upregulated and secreted proteins were present in 9 endothelial ADRC subsets including endothelial progenitor cells in the heterogenous non-cultured ADRCs. Our data thus suggest that the vascular benefit of using ADRCs in regenerative medicine is dictated by CD31+ ADRCs, which likely represent an improved alternative to heterogenous ADRCs as well as ASCs when aiming for vascular repair in cell therapy.
2023-10-24 | PXD040388 | Pride
Project description:In order to assess whether there were differences in gene expression between the polyclonal CD31+ and the polyclonal CD31- cell populations of adipose-derived adult stem cells (ADASCs), we wanted to identify possible genes that were differentially expressed between these two cell populations. To that end, RNA was isolated from polyclonal CD31+ and the polyclonal CD31- ADASCs from three different donors and analyzed using the Affymetrix Microarray HG-U133A. Then, using the Affymetrix program MAS 5.0 we performed three comparisons and could identify differentially expressed transcripts common between the three donors, using the Affymetrix program DMT 3.0.
2004-09-27 | E-MEXP-167 | biostudies-arrayexpress
Project description:The atypical chemokine receptor 4 (ACKR4)-expressing spleen endothelial cells (ECs) form a three-dimensional sinusoidal network connected via shunts to the marginal sinus and tightly surrounds the outer perimeter of the marginal zone. To better define this new vascular compartment within the red pulp of the spleen, were sorted CD31+ACKR4+ and CD31+ACKR4- EC populations, routinely yielding 92-98% cell purity and analyzed their transcriptional profiles.
2022-03-01 | GSE171335 | GEO
Project description:We performed single cell RNA seq analysis of cells isolated from mouse livers (CD45-negative and CD31-negative cells)
2022-09-28 | GSE192637 | GEO
Project description:Adipose-derived MSCs (AMSC) are currently utilized in clinical trials for various diseases including osteoarthritis, amyotrophic lateral sclerosis, and multiple system atrophy. Whilst AMSCs may be defined by the surface expression of classical markers including CD44, CD90, CD105, and absence of CD45, these cells may exhbit donor-to-donor differences in differentiation potential. In this study we evaluated the expression of CD36 amongst AMSCs and utilized magnetic cell sorting to enrich for CD36+ cells. Whole transcriptome RNA-sequencing was performed on unsorted, CD36+ enriched, and CD36+ depleted cells to determine gene expression difference between these populations of cells. CD36 sorted or unsorted cells were then plated and maintained in growth medium. Cells were expanded for 2 passages and passage 8 cells were plated for RNA-sequencing analysis. Trizol reagent was used to harvest cells when they were proliferating cells (~80%) or 100% confluent cells.
2021-11-28 | GSE189525 | GEO
Project description:To investigate the role of cd36 on CD8 T cells,we did RNAseq to find the difference between CD36 ko and WT CD8 T Cells
2021-03-10 | GSE151160 | GEO
Project description:Monocytes and macrophages as components of innate immunity are critical for both homeostasis and inflammation. The scavenger receptor CD36, highly expressed in macrophages, promotes immunological responses mediated by recognition of molecular patterns on pathogens or endogenous ligands on apoptotic cells. CD36 mediated lipid uptake also allows metabolic adaptations that influence macrophage phenotype and polarization. CD36 binds diverse lipids including fatty acids and various lipoproteins, which could exert differential effects on macrophage conversion. Previous studies reported opposite outcomes due to CD36-mediated lipid uptake; macrophages converted to either an inflammatory or an alternatively activated phenotype. To determine the role of this receptor in vivo in the presence of physiological lipid sources, we created macrophage-specific CD36 knockout mice. Using zymosan-induced peritonitis to activate immune cells, we show through single cell RNA sequencing analysis that a broad variety of resident and infiltrated immune cells are present in the peritoneum 72h after the initial stimulus. CD36 deficiency did not affect the numbers of cells during the infiltration and resolution phases, but CD36 deficiency altered the macrophage transcriptome. Pathways related to innate immunity, antigen presentation and oxidative phosphorylation were upregulated in macrophages with CD36 deficiency, whereas those related to efferocytosis, adaptive immunity and B cell activation were downregulated. Despite these gene changes, neither immunoglobulin production nor peritoneal efferocytosis was altered by macrophage CD36 deficiency, nor were there changes in the numbers of circulating white blood cells. Thus, CD36 deficiency does not reduce the inflammatory phenotype of induced peritoneal macrophages.
2024-05-31 | GSE210795 | GEO
Project description:BACKGROUND & AIMS: The scavenger receptor CD36 has versatile immuno-metabolic actions. CD36 is abundantly expressed in the small intestinal epithelium but its impact on gut homeostasis is unknown. METHODS: Wild type (WT) and CD36-null (CD36KO) mice were fed a chow diet and small intestinal morphology assessed by immunohistochemistry and electron microscopy (EM). Inflammation was evaluated from neutrophil infiltration, expression of cytokines and toll-like receptors. Barrier integrity was determined using FITC-dextran and circulating lipopolysaccharide (LPS). Enterocyte (Ent-CD36KO) and endothelial (EC-CD36KO) CD36 null mice were generated to test contribution of epithelial versus endothelial CD36 to the intestinal phenotype. RESULTS: The small intestine of CD36KO mice fed a chow diet showed abnormal remodeling of the extracellular matrix (ECM) with altered expression of ECM and junction proteins. Hypertrophy of cell junctions and basement membranes was observed by EM. The CD36KO intestines displayed neutrophil infiltration, inflammation and compromised barrier function. Systemic leukocytosis and neutrophilia were present in CD36KO mice and there was 80% reduction of anti-inflammatory Ly6Clow monocytes important for ECM regulation and tissue repair. Bone marrow transplants supported primary contribution of tissue injury in initiation of inflammation. Studies with Ent-CD36KO mice did not support a major contribution of enterocyte CD36 while endothelial CD36 deficiency associated with neutrophil infiltration, aberrant expression of tight junctions and inflammation in the small intestine. CONCLUSION: CD36 is important for maintenance of barrier function in the small intestine. CD36 deletion causes ECM remodeling with collagen accumulation, depletion of the Ly6Clow monocyte subset and chronic inflammation. Endothelial but not enterocyte CD36 loss is a significant contributor to the spontaneous inflammation.
2016-10-01 | GSE73569 | GEO