ALL TISSUES CONTROLS
Across the body
Explore brain and broad-tissue references side by side. Filter tissues and compare their endothelial populations.
Explore all tissues →HUMAN sc/snRNA-SEQ · ATLAS OVERVIEW
A collection of human endothelial single-cell and single-nucleus references.
Explore tissues, vascular cell types and genes while preserving each study’s context.
ATLAS SNAPSHOT · ALL TISSUES CONTROLS
Current retained endothelial subsets in the current sc/snRNA-seq release.
ALL TISSUES CONTROLS
Explore brain and broad-tissue references side by side. Filter tissues and compare their endothelial populations.
Explore all tissues →BRAIN CONTROLS
Examine brain endothelial expression by broad and specific region, age and vascular cell type.
Explore brain controls →GLIOBLASTOMA
Explore the available tumor-associated endothelial cohorts alongside separately labeled reference and adjacent tissues.
Explore tumor cohorts →Each study retains its own embedding and author annotations. Broad cell types and brain regions provide common groupings. Expression and detection rates remain study-specific. Source explorers retain independent embeddings; the separate Harmonized ECs pilot adjusts embedding coordinates only.
This current sc/snRNA-seq release includes every available source feature in the approved endothelial subsets. Each release is validated and updated independently of the bulk RNA-seq atlases.
The Meninges section provides separate endothelial and non-endothelial views of the same eligible human reference cohorts. Vinsland/Linnarsson is a prenatal developmental reference; Wang uses non-tumor surgical dura; Kearns/Iatrou remains private pending redistribution permission and is not included in the public explorers. These cohorts are not equivalent healthy adult controls. Author-labeled neural and adjacent-tissue populations remain visible in the non-EC view. Broad non-EC families use source annotations or explicitly documented Atlas marker-based inference when author cell labels are unavailable. Missing author labels remain marked as unavailable. EC and non-EC selections do not overlap; uncertain identities are excluded where needed. Published coordinates are retained where available; recomputed EC-only or non-EC-only UMAPs are labeled on each study.
The separate Harmonized ECs explorer selects adult control/reference arterial, capillary and venous populations after independent AtlasID review. Its experimental joint UMAP uses full-gene PCA and study correction within tissue. Original expression remains uncorrected. Eligibility exclusions and diagnostic limitations are documented in that explorer; study-specific views retain their original coordinates.
Cell Type Broad (AtlasID) combines author-supported mappings with explicitly marked atlas inferences. When source labels lack vessel detail, Atlas-inferred assignments use coherent marker programs and reference support within each study, tissue and assay. Author labels remain unchanged. Endocardial and arteriovenous transitions remain distinct. Other EC types/states includes noncanonical identities and populations without sufficient evidence for a broad vessel assignment; original labels and review reasons are retained.
Cohorts and ages. We retain study-defined endothelial cohorts and document their selection criteria. Reference, non-tumor and tumor-adjacent samples are distinguished; reference status does not imply a disease-free donor. Ages retain their source precision: exact ages, reported ranges or age bins. Bin boundaries are not exact youngest and oldest ages. Missing ages remain unavailable and are not estimated.
Annotations and provenance. Source annotations remain available. Labels marked author are source-derived; AtlasID labels identify our harmonized groupings or documented atlas inferences. Conflicting or uncertain annotations are recorded rather than silently resolved. Tissue display names may be standardized. Source versions, eligibility, mapping evidence and known cohort overlap are retained in each dataset's provenance; reused cohorts are not independent replication.
Expression and detection. Raw counts are normalized per cell or nucleus across all available source features to 10,000 counts (CP10K). Xie 2024 author-CP10K expression is preserved without re-normalization. UMAP expression uses log1p(CP10K), with a shared scale capped at the positive-value 99th percentile of visible cells. This display cap does not change counts. Expression bars average within each donor, then weight represented donors equally. Detection bars apply the same weighting to the percentage of cells with nonzero counts. Missing groups are unavailable, not zero; donors without selected cells are excluded.
Embeddings and comparisons. Each study retains its own coordinate space. Published embeddings are used where suitable; recomputed EC-only UMAPs are explicitly labeled and their parameters recorded. Filtering does not recompute UMAPs. Source explorers are not batch-integrated. The experimental Harmonized ECs view adjusts embedding coordinates only; expression remains uncorrected. Normalization does not remove assay, sampling or study effects, and these descriptive plots do not establish differential expression.
Explicit author vessel labels take priority. For generic labels, AtlasID review looks for a discriminating marker plus complementary markers and reference agreement. Donor coverage and clustering consistency inform review; low donor numbers or a lack of enrichment over neighboring ECs do not automatically prevent assignment. Ambiguous or conflicting identities remain Other EC types/states. These are population-level Atlas inferences, with original author annotations retained.
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Explore endothelial cells from primary brain tumors and brain metastases.
Tumor datasets have not been added yet. Wälchli is the first planned study.
Loading reference metadata…
Each study retains its own embedding and source annotations. Cohorts from the same study may share an embedding; separately labeled reference and tumor-adjacent tissues remain distinct. Expression differences are descriptive and are not batch-corrected. Only cohorts included in the current public release are available below.
Scroll to zoom · Drag to pan · Double-click to reset. Each study retains its own coordinate space.
76,125 cells · 9 donors
Ages: 15–69 years
Source-defined controls
24,982 nuclei · 8 donors
Ages: 58–93 years*
No cognitive impairment controls
4,652 nuclei · 196 donors
Recorded ages: 70–108 years*
Author-defined non-AD controls
73,195 cells · 21 donors
Ages: 26–74 years
Normal samples
38,665 cells · 62 donors
Age bins: 0–5 to 75–80 years*
Author-defined healthy reference
25,581 nuclei · 16 donors
Age bins: 21–40 to 61–70 years*
GTEx reference tissues
4,950 nuclei · 4 donors
Ages: 29–60 years
Source-defined reference controls
1,756 nuclei · 11 donors
Ages: 15–22 years · age ≥15 subset
Healthy distal tissue · epilepsy surgery
49,999 cells · 8 individuals
Ages: loading
Tumor · FACS endothelial compartment
Bars: mean of donor percentages · Dots: donors · 0–100%
Bars: mean of donor means · Dots: donors · CP10K · Shared axis
Uncorrected expression: tissue and study effects remain mixed.
Groups are shown with a separate bar for each contributing study. Detection is affected by capture sensitivity; expression has not been batch corrected.
| Tissue (author) | Study | Mean CP10K | Cells | Donors | Mean donor % detected |
|---|
Applies to region composition and region-colored UMAPs. Choose broad or specific bar grouping separately above. Cerebral cortex combines specified cortical areas (including entorhinal cortex) and cortex with an unspecified lobe; hippocampus stays separate. Temporal-lobe-only annotations remain separate because the sampled subregion is unresolved.
Cell / nucleus counts and percentages within each study’s current selection; donor labels may repeat across regions. Missing region annotations are shown explicitly. These proportions describe recovered cells, not anatomical abundance.
Paper-derived cohort locations: Wälchli controls are temporal lobe; Barnett’s Winkler-derived brain cells are cerebral cortex (lobe unspecified). These are cohort-level assignments; finer sample locations have not been established.
How the atlas handles annotations, ages and expression
Wälchli glioblastoma: author FACS CD31+/CD45− endothelial compartment, retaining every EC_clusters annotation, including EndoMT, Stem-to-EC, proliferating and mitochondrial states. These states map to Other unless they carry an explicit vascular class. Controls reuse the existing source-defined adult cohort, including age 15. No fetal, AVM or unsorted non-endothelial cells are added from Wälchli.
Bejarano: all 15,246 cells from the final author EC-only object, separated by disease category. Arteries 1/2, Capillaries and Veins map to their corresponding broad classes; Angiogenic, Interferon and Proliferative stay Other. The non-tumor cohort is one epilepsy surgical reference, and the IDH-mutant cohort is one individual. Reported ages are linked for all retained EC participants from Table S1, worksheet (A) Seq. Precise brain regions, treatment status and metastasis primary sites are not annotated here. Non-tumor and metastasis cells were reused by the authors from Bejarano 2024 and are represented only once here. The separate Wälchli/Xie integration used in the paper is not imported.
Xie 2024: all 57,324 author-annotated ECs, exactly matched to the author expression object by individual, condition and barcode. Adjacent non-malignant tissue (29,810 cells; 7 individuals), IDH-mutant lower-grade glioma (21,222 cells; 3 individuals), and GBM (6,292 cells; 3 individuals) retain eight author labels. GBM-EC Type 1/2 and Inflamatory EC map to Other. Expression uses author log1p(CP10K) converted back to CP10K without a second normalization; the released counts slot is not raw counts. The EC-only CSV provides display coordinates; the all-vascular object UMAP is not used. Ages, precise regions and treatment status are unavailable in the released cell metadata. Tumor-adjacent tissue is shown with controls/non-tumor references in the bar selector but retains its distinct label. Some individuals contribute paired peripheral/tumor specimens; dots are anonymous and no paired statistical test is performed.
Nomura 2025 / GBM-CARE: 5,459 author-annotated endothelial nuclei from 109 samples. Primary GBM (2,258 nuclei), first recurrence (2,630), and second recurrence (571) remain separate cohorts. All five author functional states are preserved and map to Other because they do not establish arterial, capillary or venous identity. Coordinates are a recomputed EC-only UMAP, shared across these cohorts, without batch integration. There is no healthy reference cohort. Clinical locations are tumor locations; three nuclei originate from a specimen labeled Spine. Age at initial diagnosis is available privately, but sampling age is not inferred. Nomura and the companion Spitzer paper represent the same cohort and are included once.
Abdelfattah 2022 via GBmap: 1,287 GBmap-annotated endothelial cells, split into 1,031 primary and 256 recurrent GBM cells. The source original-label field is unknown; arterial/capillary/venous identity is unresolved and maps to Other. Primary and recurrent panels share a recomputed EC-only UMAP without batch correction. There is no internal non-tumor cohort: non-malignant cells inside tumor specimens are not healthy controls. Clinical Supplementary Data 1 and GBmap were checked; ages are unavailable. Broad and specific regions describe tumor locations, not verified cortical dissections. CP10K uses all 25,987 features available in this GBmap release. GBmap is the distribution and annotation source; this is one Abdelfattah cohort, not an additional independent GBmap study.
UMAPs retain separate study coordinate frames; Nomura uses a recomputed EC-only embedding. GBM anatomical subregions and treatment status are not supplied by this downloaded metadata, so they are not inferred. Values are CP10K using all available source features in each cohort, with anonymous equal-donor summaries. The feature sets may differ. Donor IDs and original source metadata stay private.